ReviewFrontiers in immunology2025
Regulatory T cells: a promising new therapeutic target in ventricular remodeling after myocardial infarction.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Ginsenoside Rg2 fromMolecules (Basel, Switzerland) · 2026Review
- Fate-mapping infiltrating monocytes following experimental myocardial infarction reveals differentiation trajectories in the infarcted heart.The Journal of clinical investigation · 2026Article
- Review
- Review
- Deletion of STIM1 in Treg cells protects against lung fibrosis and associated cardiovascular complications in a pre-clinical mouse model.Redox biology · 2026Article
- Immune Mechanisms in Myocardial Remodeling Following Myocardial Infarction: Focusing on Regulatory Networks of T Cell Responses.Journal of inflammation research · 2026Review
- Modified mRNA-Based Therapeutic Strategies for Myocardial Ischemia-Reperfusion Injury.International journal of molecular sciences · 2025Review
- Association of Pan-Immune-Inflammation Value with All-Cause and Cardiovascular Mortality in Survivors of Myocardial Infarction: NHANES 2001-2018 Analysis.Journal of cardiovascular development and disease · 2025Article
- Nanoparticle-based drug delivery systems targeting inflammatory immune mechanisms in acute myocardial infarction: current advances and perspectives.Frontiers in cardiovascular medicine · 2025Review
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Authors and funding
3 authors.
Funding
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Abstract
Myocardial infarction (MI) is one of the leading causes of death worldwide. It is triggered by thrombosis or vascular occlusion. After MI, damaged cardiomyocytes are replaced by scar tissue, leading to systolic and diastolic dysfunction, followed by adverse remodeling. Regulatory T cells (Tregs), as major immune cells, play a crucial role in post-MI inflammation and immunomodulation. Tregs improve cardiac remodeling after MI through various mechanisms, including inhibiting inflammatory cell infiltration, inducing anti-inflammatory macrophages, suppressing cell apoptosis, regulating fibroblast function, and promoting angiogenesis. The modulation of Tregs number or function may provide novel methods for improving post-MI remodeling. This review describes the immunoregulatory roles of Tregs, their regulatory mechanisms in post-MI ventricular remodeling, and the prospects and challenges for clinical application. However, the exact molecular mechanisms of Tregs in ventricular remodeling remain to be investigated. Although most of the current studies are at the preclinical stage, they hold great potential for further application in the future.
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