ReviewWIREs mechanisms of disease2023
The cardiac wound healing response to myocardial infarction.
Review in WIREs mechanisms of disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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.
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
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Proteins targeting ischaemic-reperfusion injury and repair after myocardial infarction: a systematic literature review.Cardiovascular research · 2026Pooled it
- Optimized cardiac leukocyte isolation for flow cytometry enumeration and sorting.American journal of physiology. Heart and circulatory physiology · 2026Article
- Chitosan-based hydrogels for nitric oxide-mediated myocardial repair: advances and prospects.Journal of biological engineering · 2026Review
- Dynamic microRNA Signatures as Biomarkers for Cardiac Ischemia and Remodeling.International journal of molecular sciences · 2026Article
- Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026Review
- Electroacupuncture Protects Against Post-MI Heart Failure Through Autonomic Regulation and α7nAChR Activation.Cardiology research and practice · 2026Article
- Review
- Palmitoylated SARM1 targeting P4HA1 promotes collagen deposition and myocardial fibrosis: A new target for anti-myocardial fibrosis.Acta pharmaceutica Sinica. B · 2025Article
- Extracellular Vesicle-Enhanced Stem Cell Therapy in Acute Myocardial Infarction: A Case Report of Cardiac Regeneration from a Bypass Surgery.Stem cell reviews and reports · 2025Article
- Plasmapheresis as a Potential Generalizable Therapy for Myocardial Infarction.Rejuvenation research · 2025Review
- Digital Infrared Thermographic Imaging for Limb Salvage in Patients at Risk of Amputation: Prospective Observational Study.JMIR formative research · 2025Observational
- The Role of C-Reactive Protein in Acute Myocardial Infarction: Unmasking Diagnostic, Prognostic, and Therapeutic Insights.Journal of clinical medicine · 2025Review
- Innovative approaches to boost mesenchymal stem cells efficacy in myocardial infarction therapy.Materials today. Bio · 2025Review
- A Mathematical Exploration of the Effects of Ischemia-Reperfusion Injury After a Myocardial Infarction.Bioengineering (Basel, Switzerland) · 2025Article
- Spatial integration of multi-omics single-cell data with SIMO.Nature communications · 2025Article
- Myocardial Infarction Injury Is Exacerbated by Nicotine in Vape Aerosol Exposure.Journal of the American Heart Association · 2025Article
- Article
- Cardiac fibroblasts: answering the call.American journal of physiology. Heart and circulatory physiology · 2024Review
- Global IL4Rα blockade exacerbates heart failure after an ischemic event in mice and humans.American journal of physiology. Heart and circulatory physiology · 2024Observational
- Assessment of the alpha 7 nicotinic acetylcholine receptor as an imaging marker of cardiac repair-associated processes using NS14490.EJNMMI research · 2024Article
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
Abstract
Myocardial infarction (MI) is defined as evidence of myocardial necrosis consistent with prolonged ischemia. In response to MI, the myocardium undergoes a series of wound healing events that initiate inflammation and shift to anti-inflammation before transitioning to tissue repair that culminates in scar formation to replace the region of the necrotic myocardium. The overall response to MI is determined by two major steps, the first of which is the secretion of proteases by infiltrating leukocytes to breakdown extracellular matrix (ECM) components, a necessary step to remove necrotic cardiomyocytes. The second step is the generation of new ECM that comprises the scar; and this step is governed by the cardiac fibroblasts as the major source of new ECM synthesis. The leukocyte component resides in the middle of the two-step process, contributing to both sides as the leukocytes transition from pro-inflammatory to anti-inflammatory and reparative cell phenotypes. The balance between the two steps determines the final quantity and quality of scar formed, which in turn contributes to chronic outcomes following MI, including the progression to heart failure. This review will summarize our current knowledge regarding the cardiac wound healing response to MI, primarily focused on experimental models of MI in mice. This article is categorized under: Cardiovascular Diseases > Molecular and Cellular Physiology Immune System Diseases > Molecular and Cellular Physiology.
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What OpenQuestion 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 OpenQuestion graph.