摘要
肥胖引起多种细胞因子的表达和分泌失衡,导致代谢和心血管疾病的发展。相反,骨骼肌是k。现在要在扭转肥胖的不利影响方面发挥作用。已经证实脂肪组织是分泌促炎和抗炎脂肪因子的内分泌器官。s.同样的,骨骼肌从收缩的肌肉纤维中产生分泌分子,称为肌因子。最近,肌因子被认为是肥胖、代谢综合征的有益调节剂,2型糖尿病。此外,脂肪因子和肌动蛋白在脂肪组织、骨骼肌和其他器官之间的通讯中起着至关重要的作用。寻找新的脂肪酸是有益的。胰岛素和肌因子,并探索其信号通路,以确定治疗和预防心脏代谢紊乱的目标。在本文中,我们对相声的最新研究进行了综述。骨骼肌和脂肪组织之间。特别关注脂肪因子和肌因子的主要作用机制,如脂联素、脂肪细胞脂肪酸结合蛋白、C1q/TNF-等。相关蛋白,白介素-6,虹膜和成纤维细胞生长因子21。
关键词: 脂肪因子,肌因子,脂联素,白介素-6,虹膜素,代谢疾病,心血管疾病
Current Medicinal Chemistry
Title:Adipokines and Myokines: A Pivotal Role in Metabolic and Cardiovascular Disorders
Volume: 25 Issue: 20
关键词: 脂肪因子,肌因子,脂联素,白介素-6,虹膜素,代谢疾病,心血管疾病
摘要: Obesity induces an imbalance in the expression and secretion of several cytokines, which contributes to the development of metabolic and cardiovascular disorders. On the contrary, skeletal muscle is known to have a role in reversing the detrimental impact of obesity. It has been established that adipose tissue acts as an endocrine organ that secretes proinflammatory and anti-inflammatory adipokines. Similarly, skeletal muscle produces secretory molecules, called myokines, from contracting muscle fibers. Myokines were recently recognized as beneficial modulators of obesity, metabolic syndrome, and type 2 diabetes. Furthermore, adipokines and myokines play a crucial role in the communication between adipose tissue, skeletal muscle and other organs. It could be beneficial to find novel adipokines and myokines, and to explore their signaling pathways to identify targets for the treatment and prevention of cardiometabolic disorders. In this review, we summarize recent studies on cross-talk between skeletal muscle and adipose tissue. In particular, we concentrate on the major action mechanisms of adipokines and myokines, such as adiponectin, adipocyte fatty acid binding protein, C1q/TNF-related proteins, interleukin- 6, irisin, and fibroblast growth factor 21.
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Cite this article as:
Adipokines and Myokines: A Pivotal Role in Metabolic and Cardiovascular Disorders, Current Medicinal Chemistry 2018; 25 (20) . https://dx.doi.org/10.2174/0929867325666171205144627
DOI https://dx.doi.org/10.2174/0929867325666171205144627 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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