ReviewSignal transduction and targeted therapy2021
A double-edged sword of immuno-microenvironment in cardiac homeostasis and injury repair.
Review in Signal transduction and targeted therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 188 papers, 2 of them syntheses 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.
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Who cites it
188 citing papers in PubMed, 2 syntheses or guidelines pooled it, 269 citations in OpenAlex.
- Crosstalk between fibroblasts and immunocytes in fibrosis: From molecular mechanisms to clinical trials.Clinical and translational medicine · 2024Pooled it
- Cardiac repair after myocardial infarction: A two-sided role of inflammation-mediated.Frontiers in cardiovascular medicine · 2022Pooled it
- Inflammatory signalling in diabetic cardiomyopathy: molecular mechanisms and potential therapeutic strategies.Nature reviews. Cardiology · 2026Review
- Human pericardial macrophages suppress cardiac fibrosis through cystatin C signaling after myocardial infarction.JCI insight · 2026Article
- Antiviral innate immunity in myocarditis: mechanisms and emerging therapeutics.Experimental & molecular medicine · 2026Review
- Gut microbiota-activated PLCγ2 monocytes drive atrial fibrillation.Nature communications · 2026Article
- Integrated Bioinformatics and Experimental Validation of Post-Translational Modification-Related Biomarkers in Myocardial Ischemia-Reperfusion Injury.Journal of cardiovascular translational research · 2026Article
- Cardiac immunity and heart repair: Mechanism, challenge, and future direction.Chinese medical journal · 2026Review
- Established and emerging roles of lysosomal dysfunction in cardiac aging.Nature cardiovascular research · 2026Review
- Identification and validation of brown adipocyte-related key genes in ST-segment elevated myocardial infarction.Journal of cardiothoracic surgery · 2026Article
- Review
- Metabolic regulation of macrophage polarization in myocardial infarction: from mechanisms to targeted therapies.Journal of translational medicine · 2026Review
- Th1/Th17-Treg Imbalance in Asian Atrial Fibrillation: Subtype and Demographic Heterogeneity.JACC. Asia · 2026Article
- From targeted delivery to inflammation suppression: engineering plant exosomes for heart failure therapy post-infarction.Materials today. Bio · 2026Article
- Article
- Engineering cardiac regeneration using stem cells: Cellular sources, differentiation signatures, targeted delivery, and functional recovery.Regenerative therapy · 2026Review
- Spatial imprints of emergent cardiomyocyte states in the pressure-overloaded heart.bioRxiv : the preprint server for biology · 2026Article
- Vascularized Cardiac Tissue Engineering: From Advances in Biofabrication to Translational Applications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Pathological mechanisms and treatment strategies for immune checkpoint inhibitor-associated myocarditis: insights from single-cell sequencing.Basic research in cardiology · 2026Review
- Peritoneal cavity-derived GATA6Journal of advanced research · 2026Article
128 more citing papers are in PubMed but not listed here.
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 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The response of immune cells in cardiac injury is divided into three continuous phases: inflammation, proliferation and maturation. The kinetics of the inflammatory and proliferation phases directly influence the tissue repair. In cardiac homeostasis, cardiac tissue resident macrophages (cTMs) phagocytose bacteria and apoptotic cells. Meanwhile, NK cells prevent the maturation and transport of inflammatory cells. After cardiac injury, cTMs phagocytose the dead cardiomyocytes (CMs), regulate the proliferation and angiogenesis of cardiac progenitor cells. NK cells prevent the cardiac fibrosis, and promote vascularization and angiogenesis. Type 1 macrophages trigger the cardioprotective responses and promote tissue fibrosis in the early stage. Reversely, type 2 macrophages promote cardiac remodeling and angiogenesis in the late stage. Circulating macrophages and neutrophils firstly lead to chronic inflammation by secreting proinflammatory cytokines, and then release anti-inflammatory cytokines and growth factors, which regulate cardiac remodeling. In this process, dendritic cells (DCs) mediate the regulation of monocyte and macrophage recruitment. Recruited eosinophils and Mast cells (MCs) release some mediators which contribute to coronary vasoconstriction, leukocyte recruitment, formation of new blood vessels, scar formation. In adaptive immunity, effector T cells, especially Th17 cells, lead to the pathogenesis of cardiac fibrosis, including the distal fibrosis and scar formation. CMs protectors, Treg cells, inhibit reduce the inflammatory response, then directly trigger the regeneration of local progenitor cell via IL-10. B cells reduce myocardial injury by preserving cardiac function during the resolution of inflammation.
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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.