Abstract：
Cardiovascular diseases, mainly caused by atherosclerosis, are the leading causes of morbidity and mortality worldwide. Despite the discrepancies in clinical manifestations between different abnormalities, atherosclerosis shares similar pathophysiological processes, such as mitochondrial dysfunction. Cardiolipin (CL) is a conserved mitochondria-specific lipid that contributes to the cristae structure of the inner mitochondrial membrane (IMM). Alterations in the CL, including oxidative modification, reduced quantity, and abnormal localization, contribute to the onset and progression of atherosclerosis. In this review, we summarize the knowledge that CL is involved in the pathogenesis of atherosclerosis. On the one hand, CL and its oxidative modification promote the progression of atherosclerosis via several mechanisms, including oxidative stress, apoptosis, and inflammation in response to stress. On the other hand, CL externalizes to the outer mitochondrial membrane (OMM) and acts as the pivotal \"eat-me\" signal in mitophagy, removing dysfunctional mitochondria and safeguarding against the progression of atherosclerosis. Given the imbalance between proatherogenic and antiatherogenic effects, we provide our understanding of the roles of the CL and its oxidative modification in atherosclerotic cardiovascular diseases, in addition to potential therapeutic strategies aimed at restoring the CL. Briefly, CL is far more than a structural IMM lipid; broader significances of the evolutionarily conserved lipid need to be explored.
摘要：
心血管疾病,主要由动脉粥样硬化引起,是全球发病率和死亡率的主要原因。尽管不同异常之间的临床表现存在差异，动脉粥样硬化具有相似的病理生理过程，如线粒体功能障碍。心磷脂（CL）是一种保守的线粒体特异性脂质，有助于线粒体内膜（IMM）的cr结构。CL的改变，包括氧化改性，减少数量，和异常定位，有助于动脉粥样硬化的发生和进展。在这次审查中,我们总结了CL参与动脉粥样硬化发病机制的知识。一方面,CL及其氧化修饰通过多种机制促进动脉粥样硬化的进展，包括氧化应激,凋亡，和炎症对压力的反应。另一方面,CL外化到线粒体外膜（OMM），并在线粒体自噬中充当关键的“吃我”信号，去除功能失调的线粒体并防止动脉粥样硬化的进展。鉴于致动脉粥样硬化作用和抗动脉粥样硬化作用之间的不平衡，我们提供了我们对CL及其氧化修饰在动脉粥样硬化性心血管疾病中的作用的理解，除了旨在恢复CL的潜在治疗策略。简而言之，CL远不止是结构性IMM脂质；需要探索进化保守脂质的更广泛意义。
