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ACE-Triggered Hypertension Incites Stroke: Genetic, Molecular, and Therapeutic Aspects

期刊

NEUROMOLECULAR MEDICINE
卷 22, 期 2, 页码 194-209

出版社

HUMANA PRESS INC
DOI: 10.1007/s12017-019-08583-1

关键词

Stroke; Genetic variants; miRNAs; Neurons; Glial cells; Vascular smooth muscle cells

资金

  1. University Grants Commission (UGC), India

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Stroke is the second largest cause of death worldwide. Angiotensin converting enzyme (ACE) gene has emerged as an important player in the pathogenesis of hypertension and consequently stroke. It encodes ACE enzyme that converts the inactive decapeptide angiotensin I to active octapeptide, angiotensin II (Ang II). Dysregulation in the expression of ACE gene, on account of genetic variants or regulation by miRNAs, alters the levels of ACE in the circulation. Variable expression of ACE affects the levels of Ang II. Ang II acts through different signal transduction pathways via various tyrosine kinases (receptor/non-receptor) and protein serine/threonine kinases, initiating a downstream cascade of molecular events. In turn these activated molecular pathways might lead to hypertension and inflammation thereby resulting in cardiovascular and cerebrovascular diseases including stroke. In order to regulate the overexpression of ACE, many ACE inhibitors and blockers have been developed, some of which are still under clinical trials.

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