Ryanto Gusty Rizky Teguh, Suraya Ratoe, Nagano Tatsuya
Laboratory of Clinical Pharmaceutical Science, Kobe Pharmaceutical University, Kobe 658-8558, Japan.
Division of Respiratory Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan.
Antioxidants (Basel). 2023 Feb 3;12(2):372. doi: 10.3390/antiox12020372.
Pulmonary hypertension (PH) is a multi-etiological condition with a similar hemodynamic clinical sign and end result of right heart failure. Although its causes vary, a similar link across all the classifications is the presence of mitochondrial dysfunction. Mitochondria, as the powerhouse of the cells, hold a number of vital roles in maintaining normal cellular homeostasis, including the pulmonary vascular cells. As such, any disturbance in the normal functions of mitochondria could lead to major pathological consequences. The Warburg effect has been established as a major finding in PH conditions, but other mitochondria-related metabolic and oxidative stress factors have also been reported, making important contributions to the progression of pulmonary vascular remodeling that is commonly found in PH pathophysiology. In this review, we will discuss the role of the mitochondria in maintaining a normal vasculature, how it could be altered during pulmonary vascular remodeling, and the therapeutic options available that can treat its dysfunction.
肺动脉高压(PH)是一种多病因疾病,具有相似的血流动力学临床体征和右心衰竭的最终结果。尽管其病因各不相同,但所有分类中的一个相似联系是线粒体功能障碍的存在。线粒体作为细胞的动力源,在维持正常细胞内环境稳定方面发挥着许多重要作用,包括肺血管细胞。因此,线粒体正常功能的任何干扰都可能导致重大的病理后果。瓦伯格效应已被确认为肺动脉高压病症的一个主要发现,但也有其他与线粒体相关的代谢和氧化应激因素的报道,它们对肺动脉高压病理生理学中常见的肺血管重塑进展起到了重要作用。在这篇综述中,我们将讨论线粒体在维持正常血管系统中的作用,它在肺血管重塑过程中是如何被改变的,以及可用于治疗其功能障碍的治疗选择。