ArticleJournal of cellular and molecular medicine2022
Therapeutic potentials of cell death inhibitors in rats with cardiac ischaemia/reperfusion injury.
Article in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 27 papers.
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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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Who cites it
27 citing papers in PubMed, 41 citations in OpenAlex.
- Mitochondrial dysfunction-ferroptosis crosstalk drives renal fibrosis in chronic kidney disease.Renal failure · 2026Review
- Ferroptosis induces heterogeneous death profiles that are controlled by lysosome rupture.Developmental cell · 2026Article
- ALDH2 Mediated Ferroptosis Regulation in Ischemia-Reperfusion Injury.Journal of cellular and molecular medicine · 2026Review
- Radiotherapy combined with anti-PD-1 immunotherapy promotes ferroptosis-driven control of hepatocellular carcinoma.Genes and immunity · 2026Article
- Cell death forms in myocardial ischemia-reperfusion injury and their potential clinical applications.Molecular and cellular biochemistry · 2026Review
- Crosstalk between autophagy-dependent ferroptosis and PANoptosis in myocardial and cerebral ischemia-reperfusion injury: mechanisms and therapeutic implications.Frontiers in pharmacology · 2026Review
- Propofol decreases the resistance of neutrophils to Candida albicans by inhibiting ferroptosis and the cGAS-STING pathway.American journal of translational research · 2026Article
- BAK and BAX: Therapeutic Targets for Acute Myocardial Infarction and Myocardial Ischemia-Reperfusion Injury.Biology · 2025Review
- Pharmacological inhibition of apoptosis, necroptosis, and ferroptosis confers effective cardioprotection in post-myocardial infarction in rats.Scientific reports · 2025Article
- Lycium barbarum glycopeptide mitigates retinal ischemia-reperfusion injury through its anti-inflammatory, anti- senescence, and anti-apoptosis properties.Scientific reports · 2025Article
- Ferroptosis: A key regulator and potential target for tissue injury.Histology and histopathology · 2025Review
- Novel impact of metal ion-induced cell death on diabetic cardiomyopathy pathogenesis and therapy.Apoptosis : an international journal on programmed cell death · 2025Review
- Mechanisms and preventive measures of ALDH2 in ischemia‑reperfusion injury: Ferroptosis as a novel target (Review).Molecular medicine reports · 2025Review
- Different types of cell death and their interactions in myocardial ischemia-reperfusion injury.Cell death discovery · 2025Review
- Article
- Gastrodin prevents myocardial injury in sleep-deprived mice by suppressing ferroptosis through SIRT6.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Orientin promotes diabetic wounds healing by suppressing ferroptosis via activation of the Nrf2/GPX4 pathway.Food science & nutrition · 2024Article
- The role of iron overload and ferroptosis in arrhythmia pathogenesis.International journal of cardiology. Heart & vasculature · 2024Review
- Targeting ferroptosis and ferritinophagy: new targets for cardiovascular diseases.Journal of Zhejiang University. Science. B · 2024Review
- Exploring the mechanism of sesamin for the treatment of PMFrontiers in pharmacology · 2024Article
Corrections and comments
- Erratum issuedCorrigendum.2023
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Growing evidence demonstrated that cell death pathways including ferroptosis, apoptosis and necroptosis contribute to cardiac ischaemia/reperfusion (I/R) injury. We hypothesized that ferroptosis, apoptosis and necroptosis contribute differently to myocardial damage during acute cardiac I/R injury. Rats underwent cardiac I/R or sham operation. I/R-operated rats were divided into 4 groups: vehicle, apoptosis (Z-vad), ferroptosis (Fer-1) and necroptosis (Nec-1) inhibition. Rats in each cell death inhibitor group were subdivided into 3 different dose regimens: low, medium and high. Infarct size, left ventricular (LV) function, arrhythmias and molecular mechanism were investigated. Cardiac I/R caused myocardial infarction, LV dysfunction, arrhythmias, mitochondrial dysfunction, mitochondrial dynamic imbalance, inflammation, apoptosis and ferroptosis. Infarct size, LV dysfunction, mitochondrial dysfunction, apoptosis and ferroptosis were all reduced to a similar extent in rats treated with Z-vad (low and medium doses) or Fer-1 (medium and high doses). Fer-1 treatment also reduced mitochondrial dynamic imbalance and inflammation. No evidence of necroptosis was found in association with acute I/R injury, therefore Nec-1 treatment could not be assessed. Apoptosis and ferroptosis, not necroptosis, contributed to myocardial damage in acute I/R injury. Inhibitors of these 2 pathways provided effective cardioprotection in rats with I/R injury though modulation of mitochondrial function and attenuated apoptosis and ferroptosis.
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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 OpenQuestion graph.