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Aldosterone and inflammation

机译:醛固酮和炎症

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摘要

Purpose of review Aldosterone causes tissue inflammation leading to fibrosis and remodeling in the heart, vasculature, and kidney. We summarize recent data regarding the mechanism(s) through which aldosterone stimulates inflammation. Recent findings Studies elucidate the cell-specific effects of mineralocorticoid receptor activation on inflammatory cell infiltration and adhesion, and highlight the role of the macrophage in the development of vascular collagen deposition and hypertension. Activation of nuclear factor-kappaB in vascular smooth muscle cells involves a complex interplay between the angiotensin subtype 1 (AT_1) receptor and the mineralocorticoid receptor. Activation of the mineralocorticoid receptor by aldosterone stimulates an inflammatory phenotype in adipocytes and contributes to insulin resistance by increasing oxidative stress. Summary Mechanistic studies of aldosterone-induced inflammation provide the rationale for an expanded therapeutic role for mineralocorticoid receptor antagonists and aldosterone synthase inhibitors.
机译:审查目的醛固酮会导致组织发炎,导致心脏,血管和肾脏的纤维化和重塑。我们总结了有关醛固酮刺激炎症的机制的最新数据。最新发现研究阐明了盐皮质激素受体活化对炎性细胞浸润和粘附的细胞特异性作用,并强调了巨噬细胞在血管胶原沉积和高血压发展中的作用。血管平滑肌细胞中核因子-κB的激活涉及血管紧张素亚型1(AT_1)受体和盐皮质激素受体之间的复杂相互作用。醛固酮激活盐皮质激素受体会刺激脂肪细胞中的炎症表型,并通过增加氧化应激而有助于胰岛素抵抗。总结醛固酮诱发炎症的机理研究为盐皮质激素受体拮抗剂和醛固酮合酶抑制剂的扩大治疗作用提供了理论依据。

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