Category: 8. Health

  • New 3D eye model reveals causes of steroid-related glaucoma

    New 3D eye model reveals causes of steroid-related glaucoma

    The eye, like most organs, has an intricate plumbing system. Pressure builds when drainage is impaired, and this condition – glaucoma – can cause irreversible vision loss. Certain popular anti-inflammatory eye medications that contain steroids can in some cases compound the problem, although scientists have been at a loss to understand why.

    Now, Cornell researchers have identified the signaling mechanism that triggers steroid-induced glaucoma by creating a 3D “eye-on-a-chip” platform that mimics the flow of ocular fluids.

    The findings were published Aug. 27 in Nature Cardiovascular Research. The lead author is Renhao Lu, Ph.D. ’24.

    Steroid-induced glaucoma is a major clinical challenge. There’s no targeted therapy. We just say you are unlucky. There is a clear, unmet need to better understand, and prevent, this major side effect of the steroid in the clinics.”


    Esak (Isaac) Lee, senior author, assistant professor of biomedical engineering at Cornell Engineering

    Glaucoma is typically studied in animal models and simple 2D cell cultures, but those approaches often fail to capture the anatomical complexity and responsiveness of the human eye. 

    The solution from Lee’s lab, which studies lymphatic systems in different types of organs, has been to create 3D in-vitro models that can reproduce the systems’ layered structures while isolating biological and biophysical factors, all in a highly reproducible and controlled manner. Lee previously co-designed such a device that revealed a protein that jams up the necessary drainage in human skin lymphatic vessels, causing the painful swelling known as lymphedema.

    The eye’s lymphatic vessels are responsible for draining aqueous humor, a clear, water-like fluid that provides oxygen and nutrients but, when not removed, can cause intraocular pressure (IOP) to build, damaging neurons in the retina that are critical for transmitting light signals to the brain.

    Lee’s team realized the lymphatics in the eye, known as Schlemm’s canal (SC) cells, are quite different from those in the skin, lungs and other organs. These are surrounded by another cell type: trabecular meshwork (TM). Only with both cell layers working in conjunction can the lymphatic system flush the overproduced aqueous humor back into the bloodstream.

    The team built a 3D in-vitro device, known as a microphysiological system (MPS), with a double layer of TM and SC cells, with a curvature that mimicked the conduit structure of lymphatic vessels in the eye. The researchers treated the “eye-on-a-chip” with the anti-inflammatory steroid dexamethasone, which significantly impaired the drainage.

    This enabled the researchers to identify the culprit: A key receptor in TM cells, ALK5, responded to the steroid by downregulating a protein, vascular endothelial growth factor C (VEGFC), which normally loosens the endothelial junctions in SC cells, enabling fluid to pass through the endothelial wall. But that function was disrupted by ALK5/VEGFC signaling.

    “This communication causes the Schlemm’s canal junction abnormality,” Lee said. “The junctions become really thickened or tightened under the steroid, and that junction change increased the resistance of the outflow, causing this glaucoma.”

    The researchers confirmed the role of the mechanism in a mouse model. The finding opens up two paths to treating glaucoma: blocking ALK5 function; or providing additional VEGFC to the eye along with the steroid treatment.

    “We are now aiming to study other targets. There are some genes that people know are important for glaucoma, not just steroid-induced, and we could knock them out in these two cell types,” Lee said. “It’s complicated and difficult to target one cell type in conventional animal models, but in this system, we could do any genetic modification of these two cell types separately, and then combine them in the device to get a better understanding of these different mechanisms and different types of glaucoma.”

    Co-authors include postdoctoral researcher Anna Kolarzyk, Ph.D. ’25, and W. Daniel Stamer, professor of ophthalmology at Duke University.

    The researchers made use of the Cornell NanoScale Science and Technology Facility and was supported by the National Institutes of Health and the BrightFocus Foundation.

    Source:

    Journal reference:

    Lu, R., et al. (2025). Human ocular fluid outflow on-chip reveals trabecular meshwork-mediated Schlemm’s canal endothelial dysfunction in steroid-induced glaucoma. Nature Cardiovascular Research. doi.org/10.1038/s44161-025-00704-3

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  • Join ADAO’s 20th Annual Asbestos Awareness & Prevention Event

    Join ADAO’s 20th Annual Asbestos Awareness & Prevention Event

    The Asbestos Disease Awareness Organization will host its 20th annual Asbestos Awareness and Prevention Conference on September 12 and 13 in New York City at the Westin Grand Central hotel. Global experts will discuss diagnosing, treating and preventing asbestos-related diseases like mesothelioma, as well as policy, advocacy and asbestos law. 

    Linda Reinstein, ADAO co-founder and president, tells us this conference is unique. Reinstein shares, “This conference is about using what we know, advancing what we should know and getting to a learned place so we can prevent asbestos exposure.”

    The event will start at 4:30 p.m. on Friday, September 12 with a candlelight vigil at the World Trade Center Memorial. Participants will honor those who have died of 9/11-connected asbestos exposure. 

    Following the vigil, an awards and recognition ceremony will take place. Public health leaders and dedicated asbestos advocates will receive awards. The evening will also feature a special music performance from Jordan Zevon, a singer and songwriter who advocates for awareness about the dangers of asbestos.

    9/11 Ongoing Health Crisis and Dr. Selikoff’s Enduring Legacy

    This year’s event begins the day following the 24th anniversary of the September 11 attacks. The conference will focus on the ongoing public health crisis affecting first responders and recovery workers exposed to asbestos at Ground Zero. First responders like firefighters have developed serious illnesses linked to asbestos, including mesothelioma, which can take decades to appear. 

    ADAO continues to honor them and push for safer conditions for first responders and the public. Reinstein says, “Our annual conference is a place to exchange life-saving knowledge, honor those we’ve lost, and galvanize our efforts to ban asbestos and prevent exposure.” 

    The theme of the 2025 conference is “Building on Dr. Selikoff’s Legacy in Asbestos Science, Prevention and Justice.” During the 1950s, New York physician Dr. Irving Selikoff discovered a pattern of serious illnesses among asbestos workers. By 1964 his work proved the toxic mineral increased the risk of several deadly diseases. 

    Dr. Selikoff pioneered and transformed our understanding of asbestos exposure and asbestos-related diseases. Reinstein notes, “Gathering together in New York City is especially meaningful as we reflect on the legacy of Dr. Selikoff and the sacrifices of 9/11 responders.”

    Academic Session at Mount Sinai Hospital

    The academic session on September 13 will run from 9 a.m. to 5 p.m. at Mount Sinai Hospital. Leading medical professionals, scientists, legal experts and advocates will present information across multiple topics. 

    Medical experts will cover new breakthroughs in diagnosis, treatment and prevention strategies. Legal experts and advocates will discuss efforts to hold companies accountable and the push for a global asbestos ban.

    2025 ADAO Conference Agenda

    • Session 1: From Then to Now, Selikoff’s Vision and Our Journey Forward
    • Session 2: Diagnosing and Treating Asbestos-Related Diseases
    • Session 3: Prevention Is the Cure, Strategies for Exposure Reduction
    • Session 4: Dr. Irving Selikoff, Paul Brodeur and Beyond 
    • Session 5: Asbestos and the Law

    Tickets are still available for people who want to join. Visit ADAO’s official conference site to register and learn more.

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  • Intense light therapy boosts heart protection after surgery

    Intense light therapy boosts heart protection after surgery

    Intense light therapy after surgery can increase a critical protein that protects heart tissue while lowering levels of troponin, a protein indicating heart damage that’s linked to higher mortality in patients undergoing non-cardiac surgery, according to a study by researchers at CU Anschutz.

    The study was published this week in the Annals of Translational Medicine.

    The results add to a growing body of evidence showing that intense light has a healing effect on the heart and blood vessels, a finding that could help reduce the number of cardiac events that happen after surgery. Myocardial Injuries in Noncardiac Surgeries (MINS) occur in about 20% of patients and significantly increase one year mortality rates.

    The risk of myocardial injury goes up after certain surgeries and is significantly higher in patients older than 45. In tests on humans and animal models we found that intense light can significantly reduce troponin release. High levels of troponin following non-cardiac surgery can lead to death. Blocking it could be a very novel therapy for MINS – a disease without therapy.”


    Tobias de la Garza Eckle, MD, PhD, FASA, study’s senior author, professor of anesthesiology, CU Anschutz School of Medicine

    Eckle’s previous studies using rodent models have shown that bright light can strengthen the endothelium or lining of the blood vessels. The protection comes from a protein called PER2 which works with fellow protein HIF1A to boost levels of yet another protein ANGPTL4, a key player in vascular health.

    In this study, the researchers gave some patients having routine spine surgery intense light therapy for 30 minutes at sunrise for five days. The light increased ANGPTL4 levels and lowered troponin levels. Those who didn’t receive the therapy saw troponin levels increase.

    Eckle said bright light therapy increases the circadian rhythm amplitude and protects the heart before and after myocardial injury. The protection relies on the presence of the PER2 protein, but Eckle’s team found that ANGPTL4 protein therapy can protect the heart even when PER2 is missing.

    “This ANGPTL4 protein therapy could be a promising strategy to reduce myocardial injury to patients one day,” Eckle said. “We have started using intense light therapy in patients and have seen similar pathways are activated in humans as they are in animal models. A clinical trial will be necessary to understand the real impact of intense light therapy on Myocardial Injury in Noncardiac Surgery.”

    This study was funded by an R56 from the National Heart, Lung and Blood Institute.

    Source:

    University of Colorado Anschutz Medical Campus

    Journal reference:

    Bertazzo, J., et al. (2025). Intense light as potential future therapy for myocardial injury in patients after non cardiac surgery: lessons from mice and men. Annals of Translational Medicine. doi.org/10.21037/atm-25-27

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  • Estrogen supports kidney regeneration and protects women from chronic disease

    Estrogen supports kidney regeneration and protects women from chronic disease

    A new study in mice provides insights into why females in their reproductive years appear to be relatively protected from chronic kidney disease, a leading public health concern. The study reports that estrogen-regulated signaling promotes the regeneration of key filtration cells in female kidneys. The study also links pregnancy complications like preeclampsia to failures in this regenerative process. Chronic kidney disease (CKD) – which affects more than 10% of the global population – is a leading public health concern, not only because it can lead to fatal kidney failure, but also because it increases the risk of cardiovascular disease. Within the next 20 years, CKD is expected to become the fifth leading cause of death globally.

    Previous research has shown that sex differences play a notable role in disease progression: men are at higher risk for CKD, while women of reproductive age appear to be relatively protected. Although this suggests that female sex hormones, like progesterone and estrogen, may have a protective effect in the development of CKD, the mechanisms underlying the observed sex-based differences in disease susceptibility remain poorly understood.

    Through lineage tracing, single-cell RNA sequencing, and an analysis of mouse models and human tissue and urine samples, Carolina Conte and colleagues show that female kidneys possess a greater capacity to regenerate key filtering cells, called podocytes, from renal progenitor cells. The cells are regenerated through estrogen receptor–dependent signaling, which protects against kidney disease and hypertension during reproductive years. What’s more, the authors found that this effect intensified in pregnant mice as kidneys adapted to a higher workload. However, when this regenerative capability is compromised, such as in preeclampsia, mouse mothers face heightened long-term risks of kidney disease and hypertension. At the same time, their offspring are predisposed to poor nephron development, low birth weight, and later-life cardiovascular and renal problems.

    According to Conte et al., the findings indicate that preeclampsia may arise from a failure of kidney progenitor cells to supply sufficient podocytes, linking maternal kidney health directly to pregnancy outcomes. This link offers new insights into potential therapeutic opportunities.

    Source:

    American Association for the Advancement of Science (AAAS)

    Journal reference:

    Conte, C., et al. (2025) Estrogen-regulated renal progenitors determine pregnancy adaptation and preeclampsia. Science.doi.org/10.1126/science.adp4629

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  • Neutrophil peptide found to trigger dangerous heart arrhythmias

    Neutrophil peptide found to trigger dangerous heart arrhythmias

    Following injury from a heart attack, immune cells called neutrophils release a peptide that punctures stressed heart cells and destabilizes their electrical activity. This triggers life-threatening arrhythmias. These findings offer a novel explanation – and potential therapeutic target – for these deadly cardiac events. Ischemic heart disease – cardiac damage caused by narrowed coronary arteries – is among the leading causes of death worldwide. It can lead to heart attacks and sudden cardiac death. When a coronary artery becomes blocked, cardiomyocytes experience oxygen deprivation, which disrupts their ability to manage ions like sodium and calcium, leading to dangerous electrical instability and life-threatening arrhythmias, for which there are few treatment options beyond defibrillation. Most arrhythmias occur within the first 2 days after a heart attack, which coincides with the characteristic cellular inflammatory response to the cardiac injury. Neutrophils, which are recruited in high numbers during this response, are known to interfere with normal cellular electrical conduction and are implicated in unintended tissue damage. While this highlights neutrophils as a potential target for future therapies, their full role in promoting arrhythmias isn’t fully understood.

    Using mouse models of ischemic injury alongside human tissue and cell studies, Nina Kumowski and colleagues identified the peptide resistin-like molecule γ (Retnlg or RELMγ) as a key neutrophil-derived factor that promotes arrhythmias after a heart attack. According to Kumowski et al., RELMy – an antimicrobial pore-forming peptide – destabilizes heart rhythm by binding to and attacking stressed cardiomyocytes. Once bound, the peptide punctures the cardiomyocyte membranes, creating pores that alter cellular ion flux, triggering delayed depolarization, cell death, and the formation of tissue abnormalities that promote arrhythmia. In mouse models, removing RELMγ from neutrophils reduced ventricular arrhythmia 12-fold, supporting findings that the peptide drives electrical instability in the injured heart. Notably, the human homolog of this peptide, resistin (RETN), was detected in infarcted human myocardial tissue samples, and higher circulating RETN levels correlated with worse patient outcomes, highlighting its potential clinical relevance. In a related Perspective, Edward Thorp discusses the study in greater detail.

    Source:

    American Association for the Advancement of Science (AAAS)

    Journal reference:

    Kumowski, N., et al. (2025) Resistin-like molecule γ attacks cardiomyocyte membranes and promotes ventricular tachycardia. Science. https://www.science.org/doi/10.1126/science.adp7361

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  • Severe burden and treatment gaps reported for hyperemesis gravidarum

    Severe burden and treatment gaps reported for hyperemesis gravidarum

    Severe burden and treatment gaps reported for hyperemesis gravidarum | Image Credit: © Maridav – © Maridav – stock.adobe.com.

    Researchers from Flinders University have found a severe emotional and physical burden among pregnant women with extreme morning sickness, publishing their findings in PLOS One.1

    The data also indicated significant rates of considering pregnancy termination, alongside 9 in 10 pregnant women with extreme morning sickness considering not having more children. This highlights the debilitating nature of the condition and the inconsistent efficacy of common treatment methods.

    “Women are often prescribed multiple medications in an attempt to manage their symptoms, but the reality is that many of these treatments come with their own burdens,” said Luke Grzeskowiak, PhD, associate professor at Flinders University.

    Survey characteristics

    The cross-sectional online survey study was conducted to evaluate treatment usage and experiences among women with severe nausea and vomiting of pregnancy (NVP) or hyperemesis gravidarum (HG).2 Participants included women residing in Australia with prior or current NVP or HG experience.

    There were 4 parts to the study survey, which was completed online between July and September 2020. These parts included respondent characteristics, awareness, and perceived safety of treatments, characteristics of HG, and quality of life impact, and personal experiences.

    Quality of life impacts were reported on a 5-point Likert scale, with higher scores indicating a greater impact. Additional questions gauged considerations for pregnancy termination, depression and anxiety experiences, and requests for induction or elective cesarean section.

    Treatment experiences included treatment methods used, week of pregnancy beginning or stopping treatment, treatment duration, side effects, reasons for termination, and perceived efficacy of treatment on a 5-point Likert scale. Two consumer representatives and 2 clinical experts assessed the survey’s face validity.

    Onset and severity of symptoms

    There were 289 participants aged a mean of 33 years included in the final analysis. Of these, 38% were currently pregnant, 94% Caucasian, 95% married, and 87% with complete secondary education. One or more prior births were reported in 88% and not smoking in the current or prior pregnancy in 96%.

    NVP onset occurred at a median 6 weeks’ gestation, with all cases beginning during the first trimester. Weight loss during pregnancy was reported by 75% of participants, ranging from 1 to 40 kg, and with a median of 7 kg. Moderate NVP was reported in 41% of participants and severe NVP in 59%.

    A formal HG diagnosis was given to 76% of respondents, while 72% were admitted to the hospital for IV fluids during pregnancy. Difficulty eating or drinking as normal was reported by 98% and feelings of anxiety or depression because of HG symptoms by 62%. Thirty-seven percent requested labor induction because of their symptoms.

    Considering pregnancy termination was reported by 54% of respondents, and not having more children by 90%. Over half of respondents experienced significant impacts of HG on aspects of life, including social life, work, sleep, ability to undertake daily chores, ability to eat or drink, and taking care of pre-existing children.

    Complexity of medication use

    The use of at least 1 antiemetic during pregnancy was reported by all participants. A mean of 4.2 antiemetics were used, with a range of 1 to 9. Ondansetron was the most common antiemetic used by 91% of participants, followed by pyridoxine in 70%, doxylamine in 70%, metoclopramide in 69%, and ginger in 53%.

    Only 7% of respondents used a single antiemetic in pregnancy. Ginger, metoclopramide, ondansetron, and pyridoxine were initiated earlier than other treatments, at a median 6 weeks’ gestation for each antiemetic. The latest median time of initiation at 12 weeks’ gestation was reported for corticosteroids.

    The shortest durations of use were reported for ginger, metoclopramide, and prochlorperazine, at 2 to 4 weeks, while doxylamine and ondansetron had the longest median durations of 16 and 20 weeks, respectively.

    Side effects were reported in 78% of women taking doxylamine, 73% ondansetron, and 72% promethazine. Thirty-one percent taking metoclopramide ceased treatment because of side effects, vs 24% for ginger and 23% for prochlorperazine. Common side effects included constipation, sedation, and mood disorders.

    Implications

    Over half of respondents taking corticosteroids, ondansetron, and doxylamine reported the medication to be effective. However, under 10% reported efficacy for pyridoxine or ginger. This highlighted a complex landscape of medication use for severe NVP and HG.

    “We need to move away from a one-size-fits-all approach and toward personalized care that recognizes the full impact of HG,” said Caitlin Kay-Smith, study co-author and founder of Hyperemesis Australia.

    References

    1. Emotional and medical toll of extreme pregnancy nausea, with many women considering ending pregnancies. Flinders University. September 3, 2025. Accessed September 4, 2025. https://www.eurekalert.org/news-releases/1096797.
    2. Wills L, Hsiao H, Thomas A, Kay-Smith C, Henry A, Grzeskowiak LE. Assessing the burden of severe nausea and vomiting of pregnancy or hyperemesis gravidarum and the associated use and experiences of medication treatments: An Australian consumer survey. PLOS One. 2025. doi:10.1371/journal.pone.0329687

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  • Severe burden and treatment gaps reported for hyperemesis gravidarum

    Severe burden and treatment gaps reported for hyperemesis gravidarum

    Severe burden and treatment gaps reported for hyperemesis gravidarum | Image Credit: © Maridav – © Maridav – stock.adobe.com.

    Researchers from Flinders University have found a severe emotional and physical burden among pregnant women with extreme morning sickness, publishing their findings in PLOS One.1

    The data also indicated significant rates of considering pregnancy termination, alongside 9 in 10 pregnant women with extreme morning sickness considering not having more children. This highlights the debilitating nature of the condition and the inconsistent efficacy of common treatment methods.

    “Women are often prescribed multiple medications in an attempt to manage their symptoms, but the reality is that many of these treatments come with their own burdens,” said Luke Grzeskowiak, PhD, associate professor at Flinders University.

    Survey characteristics

    The cross-sectional online survey study was conducted to evaluate treatment usage and experiences among women with severe nausea and vomiting of pregnancy (NVP) or hyperemesis gravidarum (HG).2 Participants included women residing in Australia with prior or current NVP or HG experience.

    There were 4 parts to the study survey, which was completed online between July and September 2020. These parts included respondent characteristics, awareness, and perceived safety of treatments, characteristics of HG, and quality of life impact, and personal experiences.

    Quality of life impacts were reported on a 5-point Likert scale, with higher scores indicating a greater impact. Additional questions gauged considerations for pregnancy termination, depression and anxiety experiences, and requests for induction or elective cesarean section.

    Treatment experiences included treatment methods used, week of pregnancy beginning or stopping treatment, treatment duration, side effects, reasons for termination, and perceived efficacy of treatment on a 5-point Likert scale. Two consumer representatives and 2 clinical experts assessed the survey’s face validity.

    Onset and severity of symptoms

    There were 289 participants aged a mean of 33 years included in the final analysis. Of these, 38% were currently pregnant, 94% Caucasian, 95% married, and 87% with complete secondary education. One or more prior births were reported in 88% and not smoking in the current or prior pregnancy in 96%.

    NVP onset occurred at a median 6 weeks’ gestation, with all cases beginning during the first trimester. Weight loss during pregnancy was reported by 75% of participants, ranging from 1 to 40 kg, and with a median of 7 kg. Moderate NVP was reported in 41% of participants and severe NVP in 59%.

    A formal HG diagnosis was given to 76% of respondents, while 72% were admitted to the hospital for IV fluids during pregnancy. Difficulty eating or drinking as normal was reported by 98% and feelings of anxiety or depression because of HG symptoms by 62%. Thirty-seven percent requested labor induction because of their symptoms.

    Considering pregnancy termination was reported by 54% of respondents, and not having more children by 90%. Over half of respondents experienced significant impacts of HG on aspects of life, including social life, work, sleep, ability to undertake daily chores, ability to eat or drink, and taking care of pre-existing children.

    Complexity of medication use

    The use of at least 1 antiemetic during pregnancy was reported by all participants. A mean of 4.2 antiemetics were used, with a range of 1 to 9. Ondansetron was the most common antiemetic used by 91% of participants, followed by pyridoxine in 70%, doxylamine in 70%, metoclopramide in 69%, and ginger in 53%.

    Only 7% of respondents used a single antiemetic in pregnancy. Ginger, metoclopramide, ondansetron, and pyridoxine were initiated earlier than other treatments, at a median 6 weeks’ gestation for each antiemetic. The latest median time of initiation at 12 weeks’ gestation was reported for corticosteroids.

    The shortest durations of use were reported for ginger, metoclopramide, and prochlorperazine, at 2 to 4 weeks, while doxylamine and ondansetron had the longest median durations of 16 and 20 weeks, respectively.

    Side effects were reported in 78% of women taking doxylamine, 73% ondansetron, and 72% promethazine. Thirty-one percent taking metoclopramide ceased treatment because of side effects, vs 24% for ginger and 23% for prochlorperazine. Common side effects included constipation, sedation, and mood disorders.

    Implications

    Over half of respondents taking corticosteroids, ondansetron, and doxylamine reported the medication to be effective. However, under 10% reported efficacy for pyridoxine or ginger. This highlighted a complex landscape of medication use for severe NVP and HG.

    “We need to move away from a one-size-fits-all approach and toward personalized care that recognizes the full impact of HG,” said Caitlin Kay-Smith, study co-author and founder of Hyperemesis Australia.

    References

    1. Emotional and medical toll of extreme pregnancy nausea, with many women considering ending pregnancies. Flinders University. September 3, 2025. Accessed September 4, 2025. https://www.eurekalert.org/news-releases/1096797.
    2. Wills L, Hsiao H, Thomas A, Kay-Smith C, Henry A, Grzeskowiak LE. Assessing the burden of severe nausea and vomiting of pregnancy or hyperemesis gravidarum and the associated use and experiences of medication treatments: An Australian consumer survey. PLOS One. 2025. doi:10.1371/journal.pone.0329687

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  • Microplastics May Play Role in Idiopathic Pulmonary Fibrosis

    Microplastics May Play Role in Idiopathic Pulmonary Fibrosis

    Polyethylene terephthalate microplastics (PET-MPs) may initiate and exacerbate the progression of idiopathic pulmonary fibrosis (IPF), a new study found.

    The findings come as public health officials have raised concerns about the potential health implications of microplastics. The report was published in the journal Ecotoxicology and Environmental Safety.1

    Defined as plastic particles smaller than 5 mm, microplastics enter the environment via industrial emissions, plastic degradation, and household products. | Image credit: yrabota – stock.adobe.com

    While the underlying mechanisms behind the development of IPF are not yet fully understood, previous research has shown that environmental factors, including cigarette smoke and airborne particles, can contribute to the disease’s initiation and development, explained corresponding author Bing Bai, PhD, of the Fifth Affiliated Hospital of Zhengzhou University in China, and colleagues.2

    The potential role of environmental factors is an important research topic, Bai and colleagues said, because the incidence of IPF is rising swiftly. A 2015 study, for instance, found that the global incidence of IPF was rising by approximately 11% per year.3

    Bai and colleagues explored the potential role of microplastics in the rising rates of IPF.1 Defined as plastic particles smaller than 5 mm, microplastics enter the environment via industrial emissions, plastic degradation, and household products. From there, ingestion, inhalation, and dermal contact can all lead to the microplastics entering the human body.

    PET-MPs are the most common microplastics encountered in daily life, the authors explained, and there are several reasons why they may play a role in lung diseases like IPF.

    “PET-MPs can induce oxidative stress, mitochondrial damage, and inflammatory responses in pulmonary cells, contributing to chronic lung injury,” the authors wrote, adding that PET-MP particles smaller than 10 μm can penetrate the alveolar barrier and accumulate in lung tissue, leading to a fibrosis-like pathology.

    Yet, there is “scarce” research examining potential links between PET-MPs and the onset or exacerbation of IPF, the investigators noted. Bai and colleagues said they suspected that PET-MPs might contribute to IPF by modulating certain key molecular targets and signaling pathways.

    To test the hypothesis, the investigators used public databases and a toxicity-prediction tool called ProTox 3.0 to identify potential targets and analyze their potential roles in IPF. They used network toxicology, molecular docking, Mendelian randomization, and single-cell sequencing analysis.

    In the end, they identified 3 core targets through which they believe PET-MPs might aggravate IPF: AKT1, PIM1, and PIK3CD. The microplastics appear to affect metabolic, lipid, atherosclerosis, and C-type selection receptor signaling pathways, the authors said. They added that the binding affinity of PET-MPs to these core targets was “potent.”

    The lung toxicity of PET-MPs may be associated with the proteins AKT1, PIK3CD, and PIM1, the authors said, and they said AT2 and CD8+ T cells are susceptible to the fibrotic effects induced by PET-MPs.

    Bai and colleagues said the data show that prolonged exposure to microplastics is linked with the development of pulmonary interstitial fibrosis, and therefore they said it is urgent that regulators adopt better ways to track and restrict microplastics in the environment.

    “Furthermore, establishing long-term exposure databases and conducting multi-regional cohort studies will be key to assessing population-level health impacts,” they wrote.

    It will also be important to raise public awareness of the dangers of microplastics so that individuals—and their employers—can take steps to mitigate exposure.

    The authors cautioned that their work was based on modeling toxicity using publicly available databases, adding that it is very difficult to adequately replicate long-term, low-dose exposure to microplastics. They concluded their hypotheses will require validation through both in vitro and in vivo experiments.

    References

    1. Zhao W, Yang S, Hu S, Feng Y, Bai B. Polyethylene terephthalate microplastics promote pulmonary fibrosis via AKT1, PIK3CD, and PIM1: A network toxicology and multi-omics analysis. Ecotoxicol Environ Saf. Published online August 27, 2025. doi:10.1016/j.ecoenv.2025.118954

    2. Raghu G, Remy-Jardin M, Richeldi L, et al. Idiopathic pulmonary fibrosis (an update) and progressive pulmonary fibrosis in adults: an official ATS/ERS/JRS/ALAT clinical practice guideline. Am J Respir Crit Care Med. 2022;205(9):e18-e47. doi:10.1164/rccm.202202-0399ST

    3. Hutchinson J, Fogarty A, Hubbard R, McKeever T. Global incidence and mortality of idiopathic pulmonary fibrosis: a systematic review. Eur Respir J. 2015;46(3):795-806. doi:10.1183/09031936.00185114

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  • Evaluating Linkage to Care Among Patients With HIV Viremia in Los Angeles, California

    Evaluating Linkage to Care Among Patients With HIV Viremia in Los Angeles, California


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  • Cancer Breakthrough Sparks New Vaccine

    Cancer Breakthrough Sparks New Vaccine

    While it will take more work to see this approach leveraged in the clinic, the researchers are excited about the possibilities this breakthrough represents.

    “This is a huge step forward for personalized immune cancer therapy,” added Lippman.

    Additional coauthors of the study include: Xin Zhao, and Maria Trifas, from New York University Langone Health; William N. William from UC San Diego and Oncoclínicas São Paulo; Bin Liu, PhD, Raymond J. Lim, and Yushen Du from UCLA Jonsson Comprehensive Cancer Center and Yu-Jui Ho, Francisco M. Barriga, and Scott W. Lowe from Memorial Sloan Kettering Cancer Center.

    This study was funded, in part, by the National Institutes of Health (grants K99 CA266939, R01DE026644, U01CA0290479, P01 CA106451, P50 CA097007, P30 CA023100, R37CA248631, and R01HG012590), the Jane Coffin Childs Memorial Fund for Medical Research, Memorial Sloan Kettering Cancer Center (grants 5T32CA160001 and David Rubenstein Center for Pancreatic Research Pilot Project), the Gerry Metastasis and Tumor Ecosystems Center (GMTEC) (Postdoctoral Fellowship and Classic Individual Funding), the Edward P. Evans Foundation (Young Investigator Award), the Tobacco Related Disease Research Program (grant T30DT0963), the Howard Hughes Medical Institute, the Geoffrey Beene Chair for Cancer Biology, the Agilent Thought Leader Program, the UCLA Technology Development Group Innovation Fund, the NCI Early Detection Research Network (grant 1U2CCA271898), the Department of Veterans Affairs (grants 1I50CU000157), Cancer Research UK (grant C67321/ A29060), and Stand up to Cancer.

    Disclosures: Scott Lowe receives consultant fees and holding equity in Blueprint Medicines, ORIC Pharmaceuticals, Mirimus, PMV Pharmaceuticals, Faeth Therapeutics, Senescea Therapeutics and Constellation Pharmaceuticials. Steven Dubinett receives research funds from Janssen and Novartis, stock options and is on the advisory board of Lung Life AI, Inc. and Early Diagnostics, Inc. Teresa Davoli is a member of the SAB of io9 (now Acurion) and KaryoVerse therapeutics. Scott Lippman has served in an advisory capacity for, and received stock options from Sympto Health, Biological Dynamics; he is a cofounder of io9 LLC (now Acurion, Inc.); and is a co-inventor of IP related to genomic (9p) predictive biomarkers and precision immunotherapy: Title: Methods and Biomarkers in Cancer (inst) to Davoli and Lippman, PCT/U.S. Provisional Application Serial No. 63/483,237; and Title: Artificial Intelligence Architecture for Predicting Cancer Biomarkers (inst) to Lippman and Alexandrov, U.S. Provisional Application Serial No. 63/412,835, U.S. Provisional Application Serial No. 63/412,835 Title: Genetically-Defined Immune-Checkpoint Inhibitor Resistance in Aggressive Precursors of HPV– Head and Neck Squamous Cancer. All other authors report no disclosures.

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