ArticleThe Journal of clinical investigation2021
Healing and repair after myocardial infarction: the forgotten but resurgent basophil.
Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Healing mechanisms of Galectin-1 in the ischemic heart.Cell biochemistry and biophysics · 2026Review
- Transcriptional remodeling of cardiomyocytes and fibroblasts during post-myocardial infarction recovery.Scientific reports · 2026Article
- Identification of splenic IRF7 as a nanotherapy target for tele-conditioning myocardial reperfusion injury.Nature communications · 2025Article
- Crosstalk between macrophages and cardiac cells after myocardial infarction.Cell communication and signaling : CCS · 2023Review
- Metabolic changes of glycerophospholipids during the reparative phase after myocardial infarction injury.Frontiers in cardiovascular medicine · 2023Article
- Cardiac Shockwave Therapy - A Novel Therapy for Ischemic Cardiomyopathy?Frontiers in cardiovascular medicine · 2022Review
- The role of major immune cells in myocardial infarction.Frontiers in immunology · 2022Review
- First-in-human pilot trial of combined intracoronary and intravenous mesenchymal stem cell therapy in acute myocardial infarction.Frontiers in cardiovascular medicine · 2022Article
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Abstract
The biphasic wound-healing response in the heart after myocardial infarction involves an initial inflammatory phase followed by a more prolonged period of inflammation resolution, tissue repair, and scar formation. Infiltrating proinflammatory Ly6Chi monocytes and monocyte-derived macrophages are key drivers of the inflammatory phase and are also the source of the locally generated reparative macrophages that promote inflammation resolution. In this issue of the JCI, Sicklinger et al. from the Leuschner laboratory uncover a salutary role for cardiac basophils in this process. The authors demonstrated that basophils promote healing and proper scar formation and also limit late cardiac remodeling by augmenting reparative macrophages in the infarcted heart, in part via basophil-derived enhancement of cardiac IL-4 and IL-13 levels. These findings underscore the potentially disproportionate (relative to cell numbers) yet essential biological effects of immune cells of low abundance on cardiac repair and remodeling, related in part to amplification of downstream macrophage responses via secreted cytokines.
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Registered trials
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