ArticleChemical research in toxicology2026
Per- and Polyfluoroalkyl Substances Induce Cardiotoxicity and Alter Protein Profiles of Extracellular Matrix, Metabolism, and Mitochondrial Function in Human Cardiomyocytes.
Article in Chemical research in toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- PFAS Exposure and Metabolic Disorders: Mechanistic Insights into Lipid and Glucose Homeostasis.Biomolecules · 2026Review
- Per- and Polyfluoroalkyl Substances Exposure and Ischemic Heart Disease: Emerging Evidence from the Literature.Antioxidants (Basel, Switzerland) · 2026Review
- Knowledge structure and thematic organization of PFAS-associated cardiac toxicity: A bibliometric analysis.Toxicology reports · 2026Article
- Review
Corrections and comments
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Authors and funding
16 authors.
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Abstract
Per- and polyfluoroalkyl substances (PFAS), common environmental contaminants, can cause cardiotoxic effects particularly during fetal development. However, the effect of combined PFAS exposure, which more closely reflects real-world environmental conditions, remains poorly understood. In this study, human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) were exposed to three common PFAS compounds─perfluorohexanesulfonic acid (PFHxS), perfluorooctanoic acid (PFOA), and perfluorodecanoic acid (PFDA)─individually or in combination (20-200 μM; consistent with serum levels reported in occupationally exposed populations). Compared with single compounds, combined PFAS exposure induced synergistic cytotoxicity, significantly reducing hiPSC-CM viability after 5 or 10 days. Sublethal combined exposure for 10 days altered mitochondrial membrane potential and mitochondrial content in a dose-dependent manner and shifted cysteine metabolism, potentially reflecting adaptation to oxidative challenge. After 14 days, combined PFAS increased vimentin, a fibroblast marker, and reduced NKX2.5, α-actinin, and cardiac troponin T, key markers of cardiomyocytes, as detected by immunocytochemistry. Proteomics further showed enrichment of pathways in extracellular matrix organization, cholesterol metabolism, and antioxidant defense, as well as downregulation of mitochondrial proteins. Consistent with changes in protein profiles related to oxidative stress and bioenergetic impairment, exposure of hiPSC-CMs to combined PFAS also increased the level of mitochondrial superoxide, reduced ATP content, and decreased cellular respiration. Together, these data demonstrate that PFAS mixtures drive mitochondrial dysfunction, oxidative stress, metabolic changes, and extracellular matrix remodeling in hiPSC-CMs, underscoring the importance of evaluating PFAS mixtures to better understand cardiac risks from environmental exposure.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.