Fig. 4

Immune cells in the heart. cTMs internalize blood-borne FITC-dextran; cTMs also have typical macrophage characteristics and phagocytose bacteria and apoptotic cells. cTMs regulate electrical conduction through CX43, and cTMs can also produce proinflammatory cytokines to induce inflammation in the aging heart and promote neutrophil infiltration. Resident NK cells reduce cardiac eosinophil infiltration. NK cells prevent the maturation and transport of inflammatory cells. Monocytes are recruited into cardiac tissue and differentiate into M1 and M2 macrophages. M1 macrophages affect the proliferation and differentiation of CMs by BMPs, and M2 macrophages are related to angiogenesis by producing VEGF. Recruited neutrophils secrete proinflammatory cytokines, which promote fibroblast differentiation and lead to sustained inflammation. DCs upregulate cardiomyocyte hypertrophy a. NKT cells secrete cytokines such as IL-10 to protect or regulate hypertrophy, cardiac remodeling and the inflammatory response induced by Ang II. Infiltrating CD4 + cells include helper T cells (Th1 and Th2), Th17 cells and Treg cells. Th1 cells reduce the fibrotic response, while Th2 and Th17 cells promote fibrosis. Th17 cells also promote inflammation and extracellular matrix remodeling, and Treg cells reduce inflammation. Mast cells promote fibrosis, angiogenesis and cardiac fibroblast proliferation and collagen synthesis through TNF-α