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血管紧张素II 2型受体(AT2R)的降压潜力与表观遗传学

Anti-Hypertensive Potential and Epigenetics of Angiotensin II type 2 Receptor (AT2R).

作者信息

Chaudhary Mayank

机构信息

Department of Biotechnology, Maharishi Markandeshwar (Deemed to be University), Mullana-Ambala-133207, Haryana, India.

出版信息

Curr Hypertens Rev. 2021;17(3):176-180. doi: 10.2174/1573402116999201209203015.

Abstract

BACKGROUND

Renin angiotensin system (RAS) is a critical pathway involved in blood pressure regulation. Octapeptide, angiotensin II (Ang II), is a biologically active compound of RAS pathway which mediates its action by binding to either angiotensin II type 1 receptor (AT1R) or angiotensin II type 2 receptor (AT2R). Binding of Ang II to AT1R facilitates blood pressure regulation, whereas AT2R is primarily involved in wound healing and tissue remodeling.

OBJECTIVES

Recent studies have highlighted the additional role of AT2R to counterbalance the detrimental effects of AT1R. Activation of angiotensin II type 2 receptor using AT2R agonist has shown the effect on natriuresis and release of nitric oxide. Additionally, AT2R activation has been found to inhibit angiotensin converting enzyme (ACE) and enhance angiotensin receptor blocker (ARB) activity. These findings highlight the potential of AT2R as a novel therapeutic target against hypertension.

CONCLUSION

The potential role of AT2R highlights the importance of exploring additional mechanisms that might be crucial for AT2R expression. Epigenetic mechanisms, including DNA methylation and histone modification, have been explored vastly with relation to cancer, but the role of such mechanisms in the expression of AT2R has recently gained interest.

摘要

背景

肾素血管紧张素系统(RAS)是参与血压调节的关键途径。八肽血管紧张素II(Ang II)是RAS途径的一种生物活性化合物,它通过与1型血管紧张素II受体(AT1R)或2型血管紧张素II受体(AT2R)结合来介导其作用。Ang II与AT1R结合有助于血压调节,而AT2R主要参与伤口愈合和组织重塑。

目的

最近的研究强调了AT2R在抵消AT1R有害作用方面的额外作用。使用AT2R激动剂激活2型血管紧张素II受体已显示出对利钠作用和一氧化氮释放的影响。此外,已发现AT2R激活可抑制血管紧张素转换酶(ACE)并增强血管紧张素受体阻滞剂(ARB)的活性。这些发现突出了AT2R作为抗高血压新治疗靶点的潜力。

结论

AT2R的潜在作用突出了探索对AT2R表达可能至关重要的其他机制的重要性。表观遗传机制,包括DNA甲基化和组蛋白修饰,已在癌症方面进行了大量研究,但此类机制在AT2R表达中的作用最近引起了关注。

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