ArticleRedox biology2021
Irisin ameliorates doxorubicin-induced cardiac perivascular fibrosis through inhibiting endothelial-to-mesenchymal transition by regulating ROS accumulation and autophagy disorder in endothelial cells.
Article in Redox biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.
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Who cites it
103 citing papers in PubMed, 191 citations in OpenAlex.
- α7-nAChR Activation is Associated with Attenuation of Cardiac Fibrosis in Ischemic Cardiomyopathy via SIRT3-Dependent Modulation of EndMT.Journal of cardiovascular translational research · 2026Article
- BMSC-derived EVs alleviate doxorubicin-induced cardiotoxicity via miR-210-3p involving the ACVR1B-SMAD3-PGC-1α signaling axis.Stem cell research & therapy · 2026Article
- Exploring the Potential Impact of Nanoparticles on Fetal Development: An Updated Review.Medicina (Kaunas, Lithuania) · 2026Review
- Nicotinamide Mononucleotide Ameliorates Myocardial Fibrosis in Diabetic Mice Possibly by Modulating SIRT3 to Deacetylate GSK3β and Thereby Reducing the Phosphorylation of Smad3.Journal of cardiovascular translational research · 2026Article
- Morroniside Attenuates Doxorubicin-Induced Cardiotoxicity by Activating the PI3K/AKT/Nrf2/HO-1 Pathway to Inhibit Ferroptosis and Oxidative Stress.Journal of biochemical and molecular toxicology · 2026Article
- HIF1α Attenuates Doxorubicin-Induced Cardiotoxicity by Activating TEX264-Associated ER-phagy.Journal of the American Heart Association · 2026Article
- Autophagic therapeutic targeting for Doxorubicin-induced cardiomyopathy.Molecular biology reports · 2026Review
- Metabolic Reprogramming-Driven Cardiovascular Immune Damage: From Glyco-Lipotoxicity and Epigenetic Memory to Multidimensional Cross-Organ Communication Networks.International journal of molecular sciences · 2026Review
- Tirzepatide attenuates doxorubicin-induced cardiotoxicity via mitochondrial function improvement.Translational cancer research · 2026Article
- Prenatal lipopolysaccharide exposure programs cardiac fibrosis via dysregulating of connexin 43 in offspring rats.Molecular medicine reports · 2026Article
- Exercise-Induced Exerkines Modulate Autophagy: Implications for Interorgan Crosstalk in the Hallmarks of Ageing.International journal of molecular sciences · 2026Review
- Exercise modulates redox homeostasis in cardiovascular and metabolic diseases: from bench to clinic.Cardiovascular diabetology · 2026Review
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- 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
- Calcific aortic valve disease: can targeting endothelial-mesenchymal transition be a new alternative to surgery?-a narrative review.Cardiovascular diagnosis and therapy · 2026Review
- FNDC5/Irisin Attenuates TGF-β-induced Fibroblast Differentiation Via AMPK/Nrf2 Signaling and Mitochondrial Stabilization in Subepithelial Fibrosis.Inflammation · 2026Article
- Chicory Extract Alleviates Anthracycline-Induced Cardiotoxicity by Inhibiting Mitochondrial Damage via the UCP2/NLRP3 Pathway.International journal of molecular sciences · 2026Article
- Doxorubicin-Induced Cardiac Remodeling: Mechanisms and Mitigation Strategies.Cardiovascular drugs and therapy · 2026Review
- Anthracycline-induced cardiorenal toxicity: from molecular mechanisms to clinical management.Frontiers in cardiovascular medicine · 2026Review
- FNDC5/Irisin-dependent renoprotection of resistance training in myocardial infarction-induced Type 2 cardiorenal syndrome.PloS one · 2026Article
43 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The dose-dependent toxicity to cardiomyocytes has been well recognized as a central characteristic of doxorubicin (DOX)-induced cardiotoxicity (DIC), however, the pathogenesis of DIC in the cardiac microenvironment remains elusive. Irisin is a new hormone-like myokine released into the circulation in response to exercise with distinct functions in regulating apoptosis, inflammation, and oxidative stress. Recent advances revealed the role of irisin as a novel therapeutic method and an important mediator of the beneficial effects of exercise in cardioprotection. Here, by using a low-dose long-term mouse DIC model, we found that the perivascular fibrosis was involved in its myocardial toxicity with the underlying mechanism of endothelial-to-mesenchymal transition (EndMT). Irisin treatment could partially reverse DOX-induced perivascular fibrosis and cardiotoxicity compared to endurance exercise. Mechanistically, DOX stimulation led to excessive accumulation of ROS, which activated the NF-κB-Snail pathway and resulted in EndMT. Besides, dysregulation of autophagy was also found in DOX-treated endothelial cells. Restoring autophagy flux could ameliorate EndMT and eliminate ROS. Irisin treatment significantly alleviated ROS accumulation, autophagy disorder, NF-κB-Snail pathway activation as well as the phenotype of EndMT by targeting uncoupling protein 2 (UCP2). Our results also initially found that irisin was mainly secreted by cardiomyocytes in the cardiac microenvironment, which was significantly reduced by DOX intervention, and had a protective effect on endothelial cells in a paracrine manner. In summary, our study indicated that DOX-induced ROS accumulation and autophagy disorders caused an EndMT in CMECs, which played a role in the perivascular fibrosis of DIC. Irisin treatment could partially reverse this phenomenon by regulating UCP2. Cardiomyocytes were the main source of irisin in the cardiac microenvironment. The current study provides a novel perspective elucidating the pathogenesis and the potential treatment of DIC.
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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.