马里斯素类似SPMs的生物合成
中文名称
通路描述
马里斯素类似SPMs的生物合成。马里斯素类似介质MaR-L1、Mar-L2和14,21-二羟基二十二碳六烯酸通常由白细胞、血小板和巨噬细胞通过此处描述的路径合成。这些特化抗炎介质（SPMs）在糖尿病皮肤伤口中生产受阻与巨噬细胞功能受损及伤口愈合延迟或缺失相关（Brem & Tomic-Canic 2007, Boniakowski et al 2017）。巨噬细胞通过未知机制在伤口愈合中发挥关键作用。它们参与炎症过程的启动（M1巨噬细胞表型）和消退（M2巨噬细胞表型）。在病理状态下，从M1表型巨噬细胞向M2表型巨噬细胞的转换可能延迟或未能发生，从而导致慢性低度炎症。这种向炎症表型倾斜的巨噬细胞表型与2型糖尿病（T2D）和糖尿病伤口不愈合的发病机制有关（Boniakowski et al 2017, Pradhan et al. 2009）。
英文描述
Biosynthesis of maresin-like SPMs Maresin-like mediators MaR-L1, Mar-L2 and 14,21-dihydroxy docosahexaenoic acids are normally synthesized by leukocytes, platelets and macrophages, via the pathways described here. Impaired production of these specialised proresolving mediators (SPMs) in diabetic skin wounds is associated with impaired macrophage function and delayed or absent wound healing (Brem & Tomic-Canic 2007, Boniakowski et al 2017). Macrophages play critical roles in wound healing by mechanisms as yet unknown. They are active in both the initiation (M1 macrophage phenotype) and the resolution (M2 macrophage phenotype) of inflammatory processes. In a pathological state, the switch from the M1 phenotype macrophage to the M2 phenotype macrophage may be delayed or fail to occur, which can result in chronic low-grade inflammation. This macrophage phenotype skewing toward an inflammatory phenotype has been implicated in the pathogenesis of type 2 diabetes (T2D) and the non-healing of diabetic wounds (Boniakowski et al 2017, Pradhan et al. 2009).
Administration of maresin-like SPMs to diabetic mice with induced wounds have been shown to act as autocrine/paracrine factors in restoring reparative functions of macrophages (Hong et al. 2014, Tian et al. 2011a, 2011b, Lu et al. 2010, Hellman et al. 2012).
Administration of maresin-like SPMs to diabetic mice with induced wounds have been shown to act as autocrine/paracrine factors in restoring reparative functions of macrophages (Hong et al. 2014, Tian et al. 2011a, 2011b, Lu et al. 2010, Hellman et al. 2012).
所含基因
6 个基因