ReviewFrontiers in cell and developmental biology2021
A Novel Insight Into the Fate of Cardiomyocytes in Ischemia-Reperfusion Injury: From Iron Metabolism to Ferroptosis.
Review in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- What is the impact of ferroptosis on diabetic cardiomyopathy: a systematic review.Heart failure reviews · 2024Pooled it
- Salidroside attenuates myocardial ischemia‑reperfusion‑induced oxidative stress and ferroptosis by promoting USP11‑mediated deubiquitination of PRDX2.International journal of molecular medicine · 2026Article
- PHLDA3 hypomethylation at the mercy of PTBP1-mediated DNMT3a decay prompts ferroptosis of cardiomyocytes to accelerate microvascular endothelial cell senescence following ischemia/reperfusion injury.Molecular and cellular biochemistry · 2026Article
- Admission ferritin in STEMI predicts long-term major adverse cardiovascular outcomes.European heart journal open · 2026Article
- Changes in iron metabolism after primary PCI in patients with STEMI and ischemia-reperfusion injury.Experimental and therapeutic medicine · 2026Article
- Extracellular Vesicles in Myocardial Infarction: Dual Role in Ferroptosis Regulation and In Vivo Imaging.Diagnostics (Basel, Switzerland) · 2026Review
- Iron-dependent ferroptosis in cardiac microvascular endothelial cells: a key link between dysregulated iron homeostasis and microcirculatory injury during myocardial ischemia-reperfusion.Frontiers in cardiovascular medicine · 2026Review
- Dihydromyricetin confers protection against myocardial ischemia-reperfusion injury by inhibiting ferroptosis through direct targeting of PPARα.Frontiers in pharmacology · 2026Article
- Dihydroorotate Dehydrogenase as a Modulator of Ferroptosis in Myocardial Ischemia-reperfusion Injury.Current molecular medicine · 2026Article
- Phase-dependent iron dysmetabolism in myocardial ischemia-reperfusion injury: From mechanisms to therapies.American heart journal plus : cardiology research and practice · 2025Review
- Ferroptosis in Cardiovascular Diseases and Ferroptosis-Related Intervention Approaches.Cardiovascular drugs and therapy · 2025Review
- New Approaches and Strategies for the Repurposing of Iron Chelating/Antioxidant Drugs for Diseases of Free Radical Pathology in Medicine.Antioxidants (Basel, Switzerland) · 2025Review
- Ferroptosis: A key regulator and potential target for tissue injury.Histology and histopathology · 2025Review
- Dioscin pretreatment ameliorates ferroptosis in cardiomyocytes after myocardial infarction via inhibiting endoplasmic reticulum stress.Molecular medicine (Cambridge, Mass.) · 2025Article
- Lipid metabolism in ferroptosis: mechanistic insights and therapeutic potential.Frontiers in immunology · 2025Review
- Gastrodin prevents myocardial injury in sleep-deprived mice by suppressing ferroptosis through SIRT6.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Ferroptosis-based advanced therapies as treatment approaches for metabolic and cardiovascular diseases.Cell death and differentiation · 2024Review
- PEDF and 34-mer peptide inhibit cardiac microvascular endothelial cell ferroptosis via Nrf2/HO-1 signalling in myocardial ischemia-reperfusion injury.Journal of cellular and molecular medicine · 2024Article
- CircBAZ1B stimulates myocardial ischemia/reperfusion injury (MI/RI) by modulating miR-1252-5p/ATF3-mediated ferroptosis.Archives of medical science : AMS · 2024Article
- Mitochondrial quality control: a pathophysiological mechanism and potential therapeutic target for chronic obstructive pulmonary disease.Frontiers in pharmacology · 2024Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemia-reperfusion injury (IRI), critically involved in the pathology of reperfusion therapy for myocardial infarction, is closely related to oxidative stress the inflammatory response, and disturbances in energy metabolism. Emerging evidence shows that metabolic imbalances of iron participate in the pathophysiological process of cardiomyocyte IRI [also termed as myocardial ischemia-reperfusion injury (MIRI)]. Iron is an essential mineral required for vital physiological functions, including cellular respiration, lipid and oxygen metabolism, and protein synthesis. Nevertheless, cardiomyocyte homeostasis and viability are inclined to be jeopardized by iron-induced toxicity under pathological conditions, which is defined as ferroptosis. Upon the occurrence of IRI, excessive iron is transported into cells that drive cardiomyocytes more vulnerable to ferroptosis by the accumulation of reactive oxygen species (ROS) through Fenton reaction and Haber-Weiss reaction. The increased ROS production in ferroptosis correspondingly leads cardiomyocytes to become more sensitive to oxidative stress under the exposure of excess iron. Therefore, ferroptosis might play an important role in the pathogenic progression of MIRI, and precisely targeting ferroptosis mechanisms may be a promising therapeutic option to revert myocardial remodeling. Notably, targeting inhibitors are expected to prevent MIRI deterioration by suppressing cardiomyocyte ferroptosis. Here, we review the pathophysiological alterations from iron homeostasis to ferroptosis together with potential pathways regarding ferroptosis secondary to cardiovascular IRI. We also provide a comprehensive analysis of ferroptosis inhibitors and initiators, as well as regulatory genes involved in the setting of MIRI.
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