ReviewJournal of molecular medicine (Berlin, Germany)2023
Molecular therapy of cardiac ischemia-reperfusion injury based on mitochondria and ferroptosis.
Review in Journal of molecular medicine (Berlin, Germany), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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.
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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.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- Cardiovascular Toxicity in Cancer Therapy: Potential Mechanisms of Ferroptosis and Treatment Strategies.Cells · 2026Review
- Salvia miltiorrhiza-Derived Vesicle-Like Nanoparticles Functionalised Hydrogel With Excellent Ability of Oxidative Stress Modulation and Anti-Cardiomyocyte Apoptosis for Sepsis-Induced Myocardial Injury.Plant biotechnology journal · 2026Article
- Yixinjiedu Formula Attenuates Pressure Overload-Induced Cardiac Dysfunction by Suppressing Ferroptosis and Restoring Mitophagy via the PINK1/Parkin Axis.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Cell death forms in myocardial ischemia-reperfusion injury and their potential clinical applications.Molecular and cellular biochemistry · 2026Review
- Interplay of cGAS-STING and ferroptosis: crosstalk, molecular mechanisms, and therapeutic prospects.Archives of toxicology · 2025Review
- Involvement of ferroptosis in metabolic dysfunction-associated steatohepatitis-related liver diseases.Journal of molecular medicine (Berlin, Germany) · 2025Review
- The role and mechanism of PGC-1α in oxLDL-induced ferroptosis of vascular endothelial cells.Atherosclerosis plus · 2025Article
- Involvement of Oxidative Stress in Mitochondrial Abnormalities During the Development of Heart Disease.Biomedicines · 2025Review
- Involvement of Oxidative Stress and Antioxidants in Modification of Cardiac Dysfunction Due to Ischemia-Reperfusion Injury.Antioxidants (Basel, Switzerland) · 2025Review
- Ferroptosis genes and ST-segment elevation myocardial infarction outcomes: A predictive signature.Heliyon · 2025Article
- Targeting Lactylation Offers Therapy to Reverse Cell Death Resistance.Drug design, development and therapy · 2025Review
- Ferroptosis, a therapeutic target for cardiovascular diseases, neurodegenerative diseases and cancer.Journal of translational medicine · 2024Review
- A bibliometric study related to the treatment of myocardial ischemia-reperfusion Injury.Journal of cardiothoracic surgery · 2024Article
- Mitochondrial Melatonin: Beneficial Effects in Protecting against Heart Failure.Life (Basel, Switzerland) · 2024Review
- CircBAZ1B stimulates myocardial ischemia/reperfusion injury (MI/RI) by modulating miR-1252-5p/ATF3-mediated ferroptosis.Archives of medical science : AMS · 2024Article
- Echinacoside ameliorates doxorubicin‑induced cardiac injury by regulating GPX4 inhibition‑induced ferroptosis.Experimental and therapeutic medicine · 2024Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive death of myocardial cells can lead to various cardiovascular diseases and even develop into heart failure, so developing ideal treatment plans based on pathogenesis is of great significance for cardiopathy. After the heart undergoes ischemia‒reperfusion (I/R), myocardial cells accumulate a large amount of peroxides, leading to mitochondrial dysfunction and inducing ferroptosis. Ferroptosis is a form of iron-dependent regulatory cell death (RCD) caused by imbalanced redox and iron metabolism that leads to severe cell damage through the accumulation of peroxides. The mechanism of ferroptosis is highly correlated with mitochondrial metabolism. Myocardial cells are rich in a large number of mitochondria, which serve as energy supply centers and are prone to producing reactive oxygen species (ROS), providing opportunities for oxidative stress caused by ferroptosis. Ferroptosis is related to various cardiovascular diseases, and potential treatment methods designed around ferroptosis may alter the pathological progression of cardiovascular diseases. Therefore, this review investigates the regulatory mechanisms of ferroptosis, exploring the close pathological and physiological connections between ferroptosis and mitochondrial and cardiac I/R injury. Targeting ferroptosis and mitochondria for intervention may be an effective plan for preventing and treating cardiac I/R injury.
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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.