Mitochondria orchestrate macrophage effector functions in atherosclerosis

Macrophages are pivotal in the initiation and development of atherosclerotic cardiovascular diseases. Recent studies have reinforced the importance of mitochondria in metabolic and signaling pathways to maintain macrophage effector functions. In this review, we discuss the past and emerging roles of macrophage mitochondria metabolic diversity in atherosclerosis and the potential avenue as biomarker. Beyond metabolic functions, mitochondria are also a signaling platform integrating epigenetic, redox, efferocytic and apoptotic regulations, which are exquisitely linked to their dynamics. Indeed, mitochondria functions depend on their density and shape perpetually controlled by mitochondria fusion/fission and biogenesis/mitophagy balances. Mitochondria can also communicate with other organelles such as the endoplasmic reticulum through mitochondria-associated membrane (MAM) or be secreted for paracrine actions. All these functions are perturbed in macrophages from mouse or human atherosclerotic plaques. A better understanding and integration of how these metabolic and signaling processes are integrated and dictate macrophage effector functions in atherosclerosis may ultimately help the development of novel therapeutic approaches.

Automated summary

This review discusses the roles of macrophage mitochondrial metabolic diversity in atherosclerosis and their potential as biomarkers. Mitochondria not only play a key role in metabolism but also serve as a signaling platform, integrating various regulations that affect macrophage functions in atherosclerosis. Understanding how these processes are integrated and influence macrophage functions may lead to the development of novel therapeutic approaches.