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In addition, macrophages and NK cells have an increased capacity for phagocytosis, chemotaxis and cytokine/chemokine secretion ( Macrophage-dependent insulin resistance leads to a decrease in glycogen synthesis and muscle protein catabolism ( The increased secretion of cytokines from islet cells leads to a decrease in insulin sensitivity and a change in glucose metabolism ( Data from experimental studies suggest that the initial protective inflammatory response catalyzing insulin resistance depends on tissue macrophages ( High glucose, advanced glycation end products and oxidized low-density lipoprotein induce the production of cytokines by tissue macrophages, including IL-1, TNF-, and fibrosis transforming growth factor and thrombosis tissue factor ( Macrophage-derived TNF- and NO are both cytotoxic and involved in vascular smooth muscle cell apoptosis and atherosclerotic plaque instability ( In addition, macrophages from patients with type 2 diabetes have an increased number of NLRP3s, leading to activation of the NLRP3 inflammasome ( All in all, the increased infiltration of adipose tissue macrophages observed in animal models and in humans with diabetes suggests that adipose tissue is one of the main sites of the chronic inflammatory response associated with obesity and type 2diabetes

Gas6-Axl signal promotes indoor VOCs exposure-induced pulmonary fibrosis via pulmonary microvascular endothelial cells-fibroblasts cross-talk