Abstract
CB1 plays a crucial role in regulating M1 polarization of BMMs in liver injury, depending on two independent signaling pathways: G(α)i/o/RhoA/NF-κB p65 and G(α)i/o/ERK1/2 pathways.
Highlights
Macrophage, as an essential component of innate immunity, has emerged as a key role in liver fibrogenesis [1, 2]
Uncontrolled M1 macrophages are associated with acute infections, insulin resistance, and obesity-associated inflammation, which may contribute to the development of diseases including cardiovascular, insulin resistance, fatty liver disease, diabetes, atherosclerosis, and cancer [2, 4,5,6] In contrast, M2 macrophages are characterized by reduced responsiveness to IL-4 and IL-13, resulting in the induction of low levels of proinflammatory mediators and in the upregulation of arginase 1 (Arg1), CD163, and CD206
We investigated the effects of CB1 on BM-derived monocyte/macrophage (BMM) polarization during liver fibrogenesis
Summary
Macrophage, as an essential component of innate immunity, has emerged as a key role in liver fibrogenesis [1, 2]. A predominance of NF-κB activation promotes M1 macrophage polarization, resulting in cytotoxic and inflammatory functions [3]. M1-polarized macrophages mediate tissue damage and initiate inflammatory responses. Uncontrolled M1 macrophages are associated with acute infections, insulin resistance, and obesity-associated inflammation, which may contribute to the development of diseases including cardiovascular, insulin resistance, fatty liver disease, diabetes, atherosclerosis, and cancer [2, 4,5,6] In contrast, M2 macrophages are characterized by reduced responsiveness to IL-4 and IL-13, resulting in the induction of low levels of proinflammatory mediators and in the upregulation of arginase 1 (Arg1), CD163, and CD206. M2-polarized macrophages play important roles in the protection of the host by decreasing inflammation and promoting tissues repair [7,8,9]. Maintaining the balance of M1–M2 type macrophages may be the key point of treating many diseases [4, 10]
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