细胞生物学
血管平滑肌
环磷酸鸟苷
生物
氧化应激
线粒体
氧化磷酸化
烟酰胺腺嘌呤二核苷酸磷酸
生物化学
一氧化氮
内分泌学
氧化酶试验
酶
平滑肌
作者
Brittany G Durgin,Adam C. Straub
标识
DOI:10.1038/s41374-018-0032-9
摘要
Vascular smooth muscle cells (SMC) play a major role in vascular diseases, such as atherosclerosis and hypertension. It has long been established in vitro that contractile SMC can phenotypically switch to function as proliferative and/or migratory cells in response to stimulation by oxidative stress, growth factors, and inflammatory cytokines. Reactive oxygen species (ROS) are oxidative stressors implicated in driving vascular diseases, shifting cell bioenergetics, and increasing SMC proliferation, migration, and apoptosis. In this review, we summarize our current knowledge of how disruptions to redox balance can functionally change SMC and how this may influence vascular disease pathogenesis. Specifically, we focus on our current understanding of the role of vascular nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOX) 1, 4, and 5 in SMC function. We also review the evidence implicating mitochondrial fission in SMC phenotypic transitions and mitochondrial fusion in maintenance of SMC homeostasis. Finally, we discuss the importance of the redox regulation of the soluble guanylate cyclase (sGC)-cyclic guanosine monophosphate (cGMP)-protein kinase G (PKG) pathway as a potential oxidative and therapeutic target for regulating SMC function.Oxidative stress and smooth muscle cells (SMCs) are major contributors to pulmonary arterial hypertension, atherosclerosis, and systemic hypertension. In this review, the authors discuss how redox balance in SMC by vascular NADPH oxidases, mitochondria bioenergetics, as well as the soluble guanylate cyclase–cyclic guanosine monophosphate–protein kinase G pathway can functionally change SMC from contractile to phenotypically diverse cells and vice versa.
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