Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, Hajipur, Bihar, India.
Curr Pharm Des. 2024;30(23):1812-1821. doi: 10.2174/0113816128303026240514111200.
In the last decade, there has been increasing evidence connecting mitochondrial dysfunction to the onset and advancement of atherosclerosis. Both reactive oxygen species (ROS) and the disruption of mitochondrial calcium (Ca) regulation have garnered significant attention due to their involvement in various stages of atherosclerosis. This abstract discusses the potential therapeutic applications of targeting mitochondrial calcium (Ca) and reactive oxygen species (ROS), while also providing an overview of their respective roles in atherosclerosis. The abstract underscores the importance of mitochondrial Ca homeostasis in cellular physiology, including functions such as energy production, cell death signaling, and maintaining redox balance. Alterations in the mitochondria's Ca handling disrupt all these procedures and speed up the development of atherosclerosis. Reactive oxygen species (ROS), generated during mitochondrial respiration, are widely recognized as significant contributors to the development of atherosclerosis. Through modulating the function of calcium ion (Ca) transport proteins, ROS can impact the regulation of mitochondrial Ca handling. These oxidative modifications lead to vascular remodeling and plaque formation by impairing endothelial function, encouraging the recruitment of inflammatory cells, and promoting smooth muscle cell proliferation. Preclinical investigations indicate that interventions aimed at regulating the production and elimination of reactive oxygen species (ROS) hold promise for mitigating atherosclerosis. Targeting mitochondrial processes represents a prospective therapeutic strategy for addressing this condition. Further research is necessary to elucidate the intricate molecular mechanisms associated with mitochondrial dysfunction in atherosclerosis and develop effective therapeutic strategies to decelerate disease progression.
在过去的十年中，越来越多的证据表明线粒体功能障碍与动脉粥样硬化的发生和发展有关。由于活性氧（ROS）和线粒体钙（Ca）调节的破坏参与了动脉粥样硬化的各个阶段，因此它们受到了极大的关注。本摘要讨论了靶向线粒体钙（Ca）和活性氧（ROS）的潜在治疗应用，同时概述了它们在动脉粥样硬化中的各自作用。摘要强调了线粒体 Ca 动态平衡在细胞生理学中的重要性，包括能量产生、细胞死亡信号和维持氧化还原平衡等功能。线粒体 Ca 处理的改变会破坏所有这些过程，并加速动脉粥样硬化的发展。活性氧（ROS）是在线粒体呼吸过程中产生的，被广泛认为是动脉粥样硬化发展的重要因素。ROS 通过调节钙离子（Ca）转运蛋白的功能，影响线粒体 Ca 处理的调节。这些氧化修饰通过损害内皮功能、促进炎症细胞募集和促进平滑肌细胞增殖，导致血管重构和斑块形成。临床前研究表明，旨在调节活性氧（ROS）产生和消除的干预措施有望减轻动脉粥样硬化。靶向线粒体过程是一种有前途的治疗策略，可以解决这种情况。需要进一步研究来阐明与动脉粥样硬化中线粒体功能障碍相关的复杂分子机制，并开发有效的治疗策略来减缓疾病进展。
