ReviewInternational journal of molecular sciences2023
Cardiomyocyte Damage: Ferroptosis Relation to Ischemia-Reperfusion Injury and Future Treatment Options.
Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 11 citations in OpenAlex.
- Dual-Metal Regulation of Cardiac Remodeling: Targeting the LOXL2-Ferroptosis Axis in Metal-Induced Cardiac Dysfunction.Cardiovascular toxicology · 2026Review
- Moxibustion alleviates autophagy and inhibits ferroptosis to improve cardiac function in rats with post-myocardial infarction heart failure.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2026Article
- Nutritional redox reprogramming in cardiometabolic diseases: alpha-lipoic acid, urolithin A, and ergothioneine as modulators of the ferroptosis-mitophagy axis and mitochondrial metabolic remodeling.Frontiers in nutrition · 2026Review
- Ferroptosis-related Biotargets and Network Mechanisms of Maslinic Acid Against Myocardial Ischemia-reperfusion Injury: An Integrated Bioinformatic and Experimental Approach.Combinatorial chemistry & high throughput screening · 2026Article
- Coq4 deficiency induces placental vascular development defects through FSP1/CoQ10 axis-mediated endothelial ferroptosis.Frontiers in cell and developmental biology · 2026Article
- Regulated Cell Death and Inflammatory Signaling in Diabetic Cardiomyopathy: Mechanisms and Therapeutic Strategies.Journal of cardiovascular translational research · 2025Review
- (+)-JQ-1 alleviates cardiac injury in myocardial infarction by inhibiting ferroptosis through the NAMPT/SIRT1 pathway.Cell death & disease · 2025Article
- Ferroptosis-related LncRNAs in diseases.BMC biology · 2025Review
- MiR-370-3p regulate TLR4/SLC7A11/GPX4 to alleviate the progression of glucocorticoids-induced osteonecrosis of the femoral head by promoting osteogenesis and suppressing ferroptosis.Journal of orthopaedic translation · 2025Article
- Ferroptosis genes and ST-segment elevation myocardial infarction outcomes: A predictive signature.Heliyon · 2025Article
- Dehydroleucodine exerts an antiproliferative effect on human Burkitt's lymphoma Daudi cells via SLC7A11-mediated ferroptosis.Frontiers in pharmacology · 2025Article
- Mitochondrial Melatonin: Beneficial Effects in Protecting against Heart Failure.Life (Basel, Switzerland) · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
About half a century ago, Eugene Braunwald, a father of modern cardiology, shared a revolutionary belief that "time is muscle", which predetermined never-ending effort to preserve the unaffected myocardium. In connection to that, researchers are constantly trying to better comprehend the ongoing changes of the ischemic myocardium. As the latest studies show, metabolic changes after acute myocardial infarction (AMI) are inconsistent and depend on many constituents, which leads to many limitations and lack of unification. Nevertheless, one of the promising novel mechanistic approaches related to iron metabolism now plays an invaluable role in the ischemic heart research field. The heart, because of its high levels of oxygen consumption, is one of the most susceptible organs to iron-induced damage. In the past few years, a relatively new form of programmed cell death, called ferroptosis, has been gaining much attention in the context of myocardial infarction. This review will try to summarize the main novel metabolic pathways and show the pivotal limitations of the affected myocardium metabolomics.
Indexed as
Identifiers
What Socratic holds
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.