Cardiovascular diseases (CVD) are the leading cause of death worldwide. Although many effective therapies exist, a substantial portion of patients remain unprotected by current measures. Recent advances in the understanding of the underpinning cause of CVD, atherosclerosis, have demonstrated the important causative role of inflammation in disease progression. Monocytes are important protagonists of atherosclerosis, and they have been shown to have elevated reliance on mitochondrial metabolism producing elevated levels of superoxides as a noxious byproduct. There exists a key link between mitochondrial superoxides production and inflammatory output in monocytes in the context of atherosclerosis. In this review we describe mitochondrial superoxide lowering strategies in order to broaden the scope of treatment strategies for CVD. We further explore strategies for more effective and selective targeting of the involved monocytes and macrophages in order to increase potency of effect and diminish side effects.

心血管疾病 (CVD) 是全球主要的死亡原因。尽管存在许多有效的疗法，但很大一部分患者仍未受到当前措施的保护。对 CVD 基础病因、动脉粥样硬化的理解的最新进展已经证明炎症在疾病进展中的重要作用。单核细胞是动脉粥样硬化的重要主角，它们已被证明对线粒体代谢的依赖增加，产生高水平的超氧化物作为有害副产物。在动脉粥样硬化的背景下，线粒体超氧化物的产生与单核细胞的炎症输出之间存在关键联系。在这篇综述中，我们描述了降低线粒体超氧化物的策略，以扩大 CVD 治疗策略的范围。