ReviewFrontiers in cardiovascular medicine2021
Cardiomyocytes Cellular Phenotypes After Myocardial Infarction.
Review in Frontiers in cardiovascular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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
54 citing papers in PubMed, 73 citations in OpenAlex.
- MicroRNA-30c-1-3p Alleviates Hypoxia-Induced Cardiomyocyte Dysfunction viaBiomedicines · 2026Article
- Empagliflozin modulates microRNA expression in human primary cardiomyocytes under CoClInternational journal of cardiology. Cardiovascular risk and prevention · 2026Article
- Modulatory Effects of Dabigatran on PAR-1 Activity and Viability in Adipose-Derived Mesenchymal Stem Cells.International journal of molecular sciences · 2026Article
- Epicardial Tcf21 facilitates cardiomyocyte dedifferentiation and heart regeneration in zebrafish.Developmental biology · 2026Article
- Bioartificial Cardiac Patches Functionalized with Apelin-13 Increase Cardiac C-Type Natriuretic Peptide Expression in Infarcted Rats.Biomedicines · 2026Article
- Machine learning-derived identification of an obesity and lipid metabolism-related genes signature for the diagnosis and molecular typing of acute myocardial infarction.Frontiers in cardiovascular medicine · 2026Article
- Post-infarction KLHL40-mediated regulation of cardiac sarcomeric integrity and function.PeerJ · 2026Article
- Mapping the Inflammation Research Landscape in Myocardial Infarction, 1995-2025: A Bibliometric Analysis of WoSCC and PubMed.Journal of inflammation research · 2026Article
- SASP-mediated cellular senescence following myocardial infarction: from spatiotemporal immune regulation to therapeutic strategies.Frontiers in immunology · 2026Review
- Administration of a novel reprogramming formula improves cardiac function and decreases cardiac fibrosis in a myocardial infarction model.JTCVS open · 2025Article
- Identification and validation of biomarkers associated with cellular senescence and demethylation in acute myocardial infarction.Scientific reports · 2025Article
- Nr4a1 modulates inflammation and heart regeneration in zebrafish.Development (Cambridge, England) · 2025Article
- Circular RNA Cdr1as Modulates Macrophage-Mediated Cardiac Reparative Function.Circulation research · 2025Article
- Cardiac repair and regeneration: cell therapy, in vivo reprogramming, and the promise of extracellular vesicles.Experimental & molecular medicine · 2025Review
- Pharmacological inhibition of apoptosis, necroptosis, and ferroptosis confers effective cardioprotection in post-myocardial infarction in rats.Scientific reports · 2025Article
- Article
- Ameliorating Myocardial Infarction by Concurrent Pyroptosis Suppression and On-Demand Oxygen Production via Functionalized Nanocarrier.ACS applied materials & interfaces · 2025Article
- The context-dependent effect of cellular senescence: From embryogenesis and wound healing to aging.Ageing research reviews · 2025Review
- Unraveling the Complex Cellular Repair Mechanisms Following Myocardial Infarction.International journal of molecular sciences · 2025Review
- Cardiomyocyte specific CD38 deletion protects heart from acute myocardial infarction by activating Sirt3 signaling pathway.Scientific reports · 2025Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite the increasing success of interventional coronary reperfusion strategies, mortality related to acute myocardial infarction (MI) is still substantial. MI is defined as sudden death of myocardial tissue caused by an ischemic episode. Ischaemia leads to adverse remodelling in the affected myocardium, inducing metabolic and ionic perturbations at a single cell level, ultimately leading to cell death. The adult mammalian heart has limited regenerative capacity to replace lost cells. Identifying and enhancing physiological cardioprotective processes may be a promising therapy for patients with MI. Studies report an increasing amount of evidence stating the intricacy of the pathophysiology of the infarcted heart. Besides apoptosis, other cellular phenotypes have emerged as key players in the ischemic myocardium, in particular senescence, inflammation, and dedifferentiation. Furthermore, some cardiomyocytes in the infarct border zone uncouple from the surviving myocardium and dedifferentiate, while other cells become senescent in response to injury and start to produce a pro-inflammatory secretome. Enhancing electric coupling between cardiomyocytes in the border zone, eliminating senescent cells with senolytic compounds, and upregulating cardioprotective cellular processes like autophagy, may increase the number of functional cardiomyocytes and therefore enhance cardiac contractility. This review describes the different cellular phenotypes and pathways implicated in injury, remodelling, and regeneration of the myocardium after MI. Moreover, we discuss implications of the complex pathophysiological attributes of the infarcted heart in designing new therapeutic strategies.
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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.