Targeting the heart-immune axis after myocardial infarction: from inflammation to immunomodulation

Figures

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  Figure 1. Response of immune cells and mediators following myocardial infarction. Five phases are shown from left to right: normal, minutes, day 1, days 3-7, and several weeks post-MI. Cell types include endothelial cells, mast cells, tissue-resident macrophages (Trem2⁺, CCR2−), neutrophils, monocytes (Ly6Chigh), CCR2⁺ pro-inflammatory macrophages, CCR2− reparative macrophages, fibroblasts, NK cells, and Tregs. Arrows and labels indicate key events: differentiation, pro-inflammatory signaling, and reparative/resolution processes. Key molecules: DAMPs, IL-1β, IL-6, TNF, CCL2, TGF-β, IL-10, VEGF. This figure integrates the single-cell-based functional state framework described in the text. Created in BioRender. Huang, L. (2026) https://BioRender.com/lvpw9fo.

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  Figure 2. Cellular components of heart-immune organ axes after myocardial infarction. The infarcted heart communicates with five major immune organs via distinct signaling pathways. Colored dashed boxes list the key immune cell types involved in each axis, based on the detailed descriptions in Sections 3.1–3.5. Arrows indicate the direction of signaling (e.g., DAMPs, cytokines, catecholamines, neural signals). HSPCs, hematopoietic stem/progenitor cells; Tregs, regulatory T cells; HPA, hypothalamu-pituitary-adrenal. The cardio-thymus axis remains partially speculative and requires further validation(Section 3.5). The cardio-lung axis, listed cell types are based on emerging evidence (Section 3.5). Created in BioRender. Huang, L. (2026) https://BioRender.com/8ut0krz.