Adipokines, Hepatokines and Myokines: Focus on Their Role and Molecular Mechanisms in Adipose Tissue Inflammation.
Adipokines, Hepatokines and Myokines: Focus on Their Role and Molecular Mechanisms in Adipose Tissue Inflammation.
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脂肪因子、肝因子和肌因子：关注它们在脂肪组织炎症中的作用和分子机制
DOI：
10.3389/fendo.2022.873699
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发表时间：
2022
影响因子：
5.2
通讯作者：
中科院分区：
文献类型：
--
作者：
脂肪组织中的慢性低度炎症(AT)是肥胖的一个标志，并导致各种代谢紊乱，如2型糖尿病和心血管疾病。炎症反应的特点是巨噬细胞的浸润和由NF-κB、JNK和NLRP3炎性小体介导的炎症通路的激活。脂肪因子、肝因子和肌因子--AT、肝脏和骨骼肌分泌的蛋白质，通过内分泌、旁分泌和自分泌途径在AT炎症中发挥调节作用。例如，肥胖与促炎脂肪因子(如瘦素、抵抗素、趋化蛋白、原颗粒蛋白、RBP4、WISP1、FABP4、PAI-1、卵泡抑素样蛋白1、MCP-1、SPARC、SPARCL1和SAA)水平升高和抗炎脂肪因子水平降低有关，如脂联素、omentin、ZAG、SFRP5、CTRP3、vaspin和IL-10。此外，一些肝细胞因子(Fetuin A、DPP4、FGF21、GDF15和MANF)和肌细胞因子(Irisin、IL-6和Del-1)也在AT炎症中发挥促炎或抗炎作用。本综述旨在提供对这些有机因子及其在AT炎症和相关代谢异常中的作用的最新了解。它强调了这些有机因子作用的分子机制及其临床意义。深入了解这些有机因子的作用和机制可以为肥胖引起的炎症提供新的和潜在的治疗靶点。
Chronic low-grade inflammation in adipose tissue (AT) is a hallmark of obesity and contributes to various metabolic disorders, such as type 2 diabetes and cardiovascular diseases. Inflammation in ATs is characterized by macrophage infiltration and the activation of inflammatory pathways mediated by NF-κB, JNK, and NLRP3 inflammasomes. Adipokines, hepatokines and myokines — proteins secreted from AT, the liver and skeletal muscle play regulatory roles in AT inflammation via endocrine, paracrine, and autocrine pathways. For example, obesity is associated with elevated levels of pro-inflammatory adipokines (e.g., leptin, resistin, chemerin, progranulin, RBP4, WISP1, FABP4, PAI-1, Follistatin-like1, MCP-1, SPARC, SPARCL1, and SAA) and reduced levels of anti-inflammatory adipokines such as adiponectin, omentin, ZAG, SFRP5, CTRP3, vaspin, and IL-10. Moreover, some hepatokines (Fetuin A, DPP4, FGF21, GDF15, and MANF) and myokines (irisin, IL-6, and DEL-1) also play pro- or anti-inflammatory roles in AT inflammation. This review aims to provide an updated understanding of these organokines and their role in AT inflammation and related metabolic abnormalities. It serves to highlight the molecular mechanisms underlying the effects of these organokines and their clinical significance. Insights into the roles and mechanisms of these organokines could provide novel and potential therapeutic targets for obesity-induced inflammation.
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影响因子：
64.5
作者：
Cao H;Gerhold K;Mayers JR;Wiest MM;Watkins SM;Hotamisligil GS
通讯作者：
Hotamisligil GS
影响因子：
8.1
作者：
Baumeier C;Schlüter L;Saussenthaler S;Laeger T;Rödiger M;Alaze SA;Fritsche L;Häring HU;Stefan N;Fritsche A;Schwenk RW;Schürmann A
通讯作者：
Schürmann A
影响因子：
7.7
作者：
Benomar Y;Gertler A;De Lacy P;Crépin D;Ould Hamouda H;Riffault L;Taouis M
通讯作者：
Taouis M
影响因子：
5.6
作者：
Schmid A;Roderfeld M;Gehl J;Roeb E;Nist A;Chung HR;Stiewe T;Karrasch T;Schäffler A
通讯作者：
Schäffler A
影响因子：
3.7
作者：
Kotnik P;Keuper M;Wabitsch M;Fischer-Posovszky P
通讯作者：
Fischer-Posovszky P