ArticleLaboratory investigation; a journal of technical methods and pathology2014
Oxidative stress mediates the conversion of endothelial cells into myofibroblasts via a TGF-β1 and TGF-β2-dependent pathway.
Article in Laboratory investigation; a journal of technical methods and pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
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84 citing papers in PubMed, 141 citations in OpenAlex.
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- PTUPB, a soluble epoxide hydrolase/cyclooxygenase‑2 dual inhibitor, reduces endothelial‑to‑mesenchymal transition and improves doxorubicin‑induced vascular and cardiac toxicity.Molecular medicine reports · 2026Article
- Camphor alleviates renal fibrosis by suppressing oxidative stress and inflammation, up-regulating SIRT1 and down-regulating NF-κB and TGF-β.Molecular and cellular biochemistry · 2026Article
- The effects of combined low-dose cadmium and deltamethrin on mitochondrial bioenergetics and metabolism in human lung fibroblasts.Toxicology reports · 2025Article
- Endothelial-to-mesenchymal transition in the central nervous system: A potential therapeutic target to combat age-related vascular fragility.The Journal of pharmacology and experimental therapeutics · 2025Review
- Endothelial to mesenchymal transition: a central mechanism in diabetes-induced vascular pathology.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Review
- Molecular Basis of Oxidative Stress-Induced Acute Kidney Injury, Kidney Fibrosis, Chronic Kidney Disease, and Clinical Significance of Targeting Reactive Oxygen Species-Regulated Pathways to Treat Kidney Disease.Frontiers in bioscience (Scholar edition) · 2025Review
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- Mechanistic insights and emerging therapeutic strategies targeting endothelial dysfunction in cardiovascular diseases.Archives of pharmacal research · 2025Review
- SCPEP1Frontiers in immunology · 2025Article
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- TGFβ2 mediates oxidative stress-induced epithelial-to-mesenchymal transition of bladder smooth muscle.In vitro cellular & developmental biology. Animal · 2024Article
- N6-methyladenosine modification of KLF2 may contribute to endothelial-to-mesenchymal transition in pulmonary hypertension.Cellular & molecular biology letters · 2024Article
- Construction of tissue-engineered vascular grafts with enhanced patency by integrating heparin, cell-adhesive peptide, and carbon monoxide nanogenerators into acellular blood vessels.Bioactive materials · 2024Article
- Endothelial to mesenchymal transition: at the axis of cardiovascular health and disease.Cardiovascular research · 2024Review
- AMPK signaling inhibits the differentiation of myofibroblasts: impact on age-related tissue fibrosis and degeneration.Biogerontology · 2024Review
24 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During the pathogenesis of systemic inflammation, reactive oxygen species (ROS) circulate in the bloodstream and interact with endothelial cells (ECs), increasing intracellular oxidative stress. Although endothelial dysfunction is crucial in the pathogenesis of systemic inflammation, little is known about the effects of oxidative stress on endothelial dysfunction. Oxidative stress induces several functions, including cellular transformation. A singular process of cell conversion is tendothelial-to-mesenchymal transition, in which ECs become myofibroblasts, thus losing their endothelial properties and gaining fibrotic behavior. However, the participation of oxidative stress as an inductor of conversion of ECs into myofibroblasts is not known. Thus, we studied the role played by oxidative stress in this conversion and investigated the underlying mechanism. Our results show that oxidative stress induces conversion of ECs into myofibroblasts through decreasing the levels of endothelial markers and increasing those of fibrotic and ECM proteins. The underlying mechanism depends on the ALK5/Smad3/NF-κB pathway. Oxidative stress induces the expression and secretion of TGF-β1 and TGF-β2 and p38 MAPK phosphorylation. Downregulation of TGF-β1 and TGF-β2 by siRNA technology abolished the H2O2-induced conversion. To our knowledge, this is the first report showing that oxidative stress is able to induce conversion of ECs into myofibroblasts via TGF-β secretion, emerging as a source for oxidative stress-based vascular dysfunction. Thus, oxidative stress emerges as a decisive factor in inducing conversion of ECs into myofibroblasts through a TGF-β-dependent mechanism, changing the ECs protein expression profile, and converting normal ECs into pathological ones. This information will be useful in designing new and improved therapeutic strategies against oxidative stress-mediated systemic inflammatory diseases.
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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 OpenQuestion graph.