Role of Endogenous Sulfur Dioxide in Regulating Vascular Structural Remodeling in Hypertension.
Role of Endogenous Sulfur Dioxide in Regulating Vascular Structural Remodeling in Hypertension.
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内源性二氧化硫在调节高血压血管结构重塑中的作用
DOI：
10.1155/2016/4529060
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发表时间：
2016
影响因子：
--
通讯作者：
Du J
中科院分区：
文献类型：
--
作者：
Liu J;Huang Y;Chen S;Tang C;Jin H;Du J
二氧化硫(SO2)是一种新兴的气体递质，被发现是在心血管系统内源性产生的。近年来，内源SO2的生理效应得到证实。血管结构重塑(VSR)是许多心血管疾病的重要病理改变，在心血管疾病的发病机制中起着至关重要的作用。本文通过检索PubMed和Medline的相关数据，综述了内源性SO2调节VSR的研究进展。在自发性高血压大鼠(SHR)和肺动脉高压大鼠中，SO2/天冬氨酸氨基转移酶(AAT)通路明显改变。SO2抑制血管平滑肌细胞(VSMC)增殖，促进细胞凋亡，抑制细胞外胶原合成但促进其降解，增强抗氧化能力，从而起到抑制VSR的作用。然而，具体的机制还需要进一步探讨。这一领域的进一步研究对于更好地了解全身高压和肺动脉高压的发病机制具有重要意义。此外，还需要临床试验来证明二氧化硫是否会成为心血管疾病的潜在治疗靶点。
Sulfur dioxide (SO2), an emerging gasotransmitter, was discovered to be endogenously generated in the cardiovascular system. Recently, the physiological effects of endogenous SO2 were confirmed. Vascular structural remodeling (VSR), an important pathological change in many cardiovascular diseases, plays a crucial role in the pathogenesis of the diseases. Here, the authors reviewed the research progress of endogenous SO2 in regulating VSR by searching the relevant data from PubMed and Medline. In spontaneously hypertensive rats (SHRs) and pulmonary hypertensive rats, SO2/aspartate aminotransferase (AAT) pathway was significantly altered. SO2 inhibited vascular smooth muscle cell (VSMC) proliferation, promoted apoptosis, inhibited the synthesis of extracellular collagen but promoted its degradation, and enhanced antioxidative capacity, thereby playing a significant role in attenuating VSR. However, the detailed mechanisms needed to be further explored. Further studies in this field would be important for the better understanding of the pathogenesis of systemic hypertension and pulmonary hypertension. Also, clinical trials are needed to demonstrate if SO2 would be a potential therapeutic target in cardiovascular diseases.
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