New take on the role of angiotensin II in cardiac hypertrophy and fibrosis.
New take on the role of angiotensin II in cardiac hypertrophy and fibrosis.
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DOI：
10.1161/hypertensionaha.111.172700
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发表时间：
2011-06
期刊：
影响因子：
--
通讯作者：
Booz GW
中科院分区：
文献类型：
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作者：
Kurdi M;Booz GW
近4年前，《高血压》杂志发表了一篇简短的综述，对当时普遍认为的血管紧张素II （Ang II）对高血压患者心脏重构相关的心肌细胞和成纤维细胞具有直接的生长促进作用提出了质疑。这篇综述令人信服地指出，认为Ang II具有“心脏营养”作用的观点主要是基于对培养细胞的研究，并没有得到转基因动物研究结果的证实。对于许多人来说，关键的信息是，在高血压中看到的心脏重塑中，Ang II并不是一个参与者。然而，在他们的结论中，作者指出，“当与其他体液、机械或病理刺激结合时，这些结果并不排除Ang II在心脏重塑中的直接作用……”事实上，最近的证据支持这样的结论，即Ang II与其他因素协同作用，在高血压引起的左心室重塑中起着重要作用。在这里，我们重点介绍了最近的一些研究，以及对内源性反调节机制的新见解，这些机制可能被用于治疗。
Nearly 4 years ago in Hypertension, a brief review was published that called into question the widely held belief at the time that angiotensin II (Ang II) has direct growthpromoting effects on cardiac myocytes and fibroblasts relevant to the development of cardiac remodeling in hypertension. 1 The review convincingly argued that the idea that Ang II was “cardiotrophic” rested largely on work with cultured cells and was not substantiated by results from genetically modified animals. For many the take-home message was that Ang II was not a player in cardiac remodeling seen in hypertension. However, in their conclusion, the authors noted that,“these results do not rule out a direct role for Ang II in cardiac remodeling when combined with other humoral, mechanical, or pathological stimuli…” 1 Indeed, recent evidence supports the conclusion that Ang II acting in concert with other factors plays an important role in the remodeling of the left ventricle produced by hypertension. Here we highlight some of these recent studies, as well as new insights into endogenous counterregulatory mechanisms that might be exploited therapeutically.