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Adiponectin and Adiponectin Receptors in Atherosclerosis.
Endocrine Reviews ( IF 22.0 ) Pub Date : 2024-08-06 , DOI: 10.1210/endrev/bnae021 Ioanna Gianopoulos 1 , Christos S Mantzoros 2, 3 , Stella S Daskalopoulou 1, 4
Endocrine Reviews ( IF 22.0 ) Pub Date : 2024-08-06 , DOI: 10.1210/endrev/bnae021 Ioanna Gianopoulos 1 , Christos S Mantzoros 2, 3 , Stella S Daskalopoulou 1, 4
Affiliation
Adiponectin is an abundantly secreted hormone that communicates information between the adipose tissue, and the immune and cardiovascular systems. In metabolically healthy individuals, adiponectin is usually found at high levels and helps improve insulin responsiveness of peripheral tissues, glucose tolerance, and fatty acid oxidation. Beyond its metabolic functions in insulin-sensitive tissues, adiponectin plays a prominent role in attenuating the development of atherosclerotic plaques, partially through regulating macrophage-mediated responses. In this context, adiponectin binds to its receptors, adiponectin receptor 1 (AdipoR1) and AdipoR2 on the cell surface of macrophages to activate a downstream signaling cascade and induce specific atheroprotective functions. Notably, macrophages modulate the stability of the plaque through their ability to switch between pro-inflammatory responders, and anti-inflammatory pro-resolving mediators. Traditionally, the extremes of the macrophage polarization spectrum span from M1 pro-inflammatory and M2 anti-inflammatory phenotypes. Previous evidence has demonstrated that the adiponectin-AdipoR pathway influences M1-M2 macrophage polarization; adiponectin promotes a shift towards an M2-like state, whereas AdipoR1- and AdipoR2-specific contributions are more nuanced. To explore these concepts in depth, we discuss in this review the impact of adiponectin and AdipoR1/R2 on 1) metabolic and immune responses, and 2) M1-M2 macrophage polarization, including their ability to attenuate atherosclerotic plaque inflammation, and their potential as therapeutic targets for clinical applications.
中文翻译:
动脉粥样硬化中的脂联素和脂联素受体。
脂联素是一种分泌丰富的激素,可在脂肪组织、免疫系统和心血管系统之间传递信息。在代谢健康的个体中,脂联素通常含量较高,有助于改善外周组织的胰岛素反应性、葡萄糖耐量和脂肪酸氧化。除了在胰岛素敏感组织中的代谢功能外,脂联素在减轻动脉粥样硬化斑块的发展方面也发挥着重要作用,部分是通过调节巨噬细胞介导的反应来实现的。在这种情况下,脂联素与其巨噬细胞细胞表面的受体脂联素受体 1 (AdipoR1) 和 AdipoR2 结合,激活下游信号级联并诱导特定的动脉粥样硬化保护功能。值得注意的是,巨噬细胞通过在促炎反应物和抗炎促消解介质之间切换的能力来调节斑块的稳定性。传统上,巨噬细胞极化谱的极端范围涵盖 M1 促炎表型和 M2 抗炎表型。先前的证据表明脂联素-AdipoR通路影响M1-M2巨噬细胞极化;脂联素促进向 M2 样状态的转变,而 AdipoR1 和 AdipoR2 的特异性贡献则更为微妙。为了深入探讨这些概念,我们在这篇综述中讨论了脂联素和 AdipoR1/R2 对 1) 代谢和免疫反应以及 2) M1-M2 巨噬细胞极化的影响,包括它们减轻动脉粥样硬化斑块炎症的能力,以及它们作为治疗药物的潜力。临床应用的治疗靶点。
更新日期:2024-08-06
中文翻译:
动脉粥样硬化中的脂联素和脂联素受体。
脂联素是一种分泌丰富的激素,可在脂肪组织、免疫系统和心血管系统之间传递信息。在代谢健康的个体中,脂联素通常含量较高,有助于改善外周组织的胰岛素反应性、葡萄糖耐量和脂肪酸氧化。除了在胰岛素敏感组织中的代谢功能外,脂联素在减轻动脉粥样硬化斑块的发展方面也发挥着重要作用,部分是通过调节巨噬细胞介导的反应来实现的。在这种情况下,脂联素与其巨噬细胞细胞表面的受体脂联素受体 1 (AdipoR1) 和 AdipoR2 结合,激活下游信号级联并诱导特定的动脉粥样硬化保护功能。值得注意的是,巨噬细胞通过在促炎反应物和抗炎促消解介质之间切换的能力来调节斑块的稳定性。传统上,巨噬细胞极化谱的极端范围涵盖 M1 促炎表型和 M2 抗炎表型。先前的证据表明脂联素-AdipoR通路影响M1-M2巨噬细胞极化;脂联素促进向 M2 样状态的转变,而 AdipoR1 和 AdipoR2 的特异性贡献则更为微妙。为了深入探讨这些概念,我们在这篇综述中讨论了脂联素和 AdipoR1/R2 对 1) 代谢和免疫反应以及 2) M1-M2 巨噬细胞极化的影响,包括它们减轻动脉粥样硬化斑块炎症的能力,以及它们作为治疗药物的潜力。临床应用的治疗靶点。