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血管紧张素转换酶抑制在对抗肾纤维化中的生物学意义。

The biological significance of angiotensin-converting enzyme inhibition to combat kidney fibrosis.

机构信息

Department of Diabetology and Endocrinology, Kanazawa Medical University, Uchinada, Ishikawa, 920-0293, Japan.

出版信息

Clin Exp Nephrol. 2015 Feb;19(1):65-74. doi: 10.1007/s10157-014-1000-3. Epub 2014 Jul 1.

Abstract

Both angiotensin-converting enzyme inhibitor (ACE-I) and angiotensin II receptor blocker have been recognized as renin-angiotensin system (RAS) inhibitors. These two RAS inhibitors are rarely recognized as drugs with distinct pharmacological effects in the clinic or most clinical trials. Some preclinical basic research and clinical trials indicate that ACE-I might display superior organ-protective effects, especially anti-fibrotic effects. Such anti-fibrotic effects of ACE-I could be associated with an endogenous anti-fibrotic peptide, N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP). In this review, we focused on the anti-fibrotic effects of RAS inhibition and the endogenous anti-fibrotic peptide AcSDKP.

摘要

血管紧张素转换酶抑制剂(ACE-I)和血管紧张素 II 受体阻滞剂都被认为是肾素-血管紧张素系统(RAS)抑制剂。这两种 RAS 抑制剂在临床上或大多数临床试验中很少被认为是具有明显药理作用的药物。一些临床前基础研究和临床试验表明,ACE-I 可能具有更好的器官保护作用,特别是抗纤维化作用。ACE-I 的这种抗纤维化作用可能与内源性抗纤维化肽 N-乙酰丝氨酰-天冬氨酰-赖氨酰-脯氨酸(AcSDKP)有关。在这篇综述中,我们重点介绍了 RAS 抑制的抗纤维化作用和内源性抗纤维化肽 AcSDKP。

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