Mitochondrial Quality Control in Macrophages during Cardiovascular Disease

Feb 25, 2026The Canadian journal of cardiology

Mitochondrial Quality Control in Immune Cells during Heart and Blood Vessel Disease

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Abstract

Mitochondrial dysfunction in macrophages is associated with chronic inflammation and tissue injury in cardiovascular disease.

Macrophages play a crucial role in regulating vascular inflammation and tissue remodeling in the cardiovascular system.
Mitochondria in macrophages integrate metabolism with immunogenic signal production, influencing inflammatory responses.
Dysregulated mitochondrial dynamics and increased oxidative stress in macrophages may exacerbate inflammation related to cardiovascular disease.
Mitochondrial quality control mechanisms, such as biogenesis and mitophagy, are essential for macrophage function and survival in cardiovascular conditions.
Current therapies like statins and SGLT2 inhibitors may improve macrophage mitochondrial quality control and reduce inflammation, potentially benefiting cardiovascular health.

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Macrophages are key cells of the innate immune system. Within the cardiovascular system, macrophages exhibit marked phenotypic plasticity, enabling them to sense local cues and regulate vascular inflammation, myocardial injury, and tissue remodeling. Mitochondria serve as multifunctional organelles in macrophages, integrating cellular metabolism with the production of immunogenic signals that shape inflammatory responses. In cardiovascular disease (CVD), mitochondrial dysfunction in macrophages drives maladaptive inflammatory responses that when unresolved, lead to chronic inflammation and tissue injury underlying adverse cardiovascular outcomes. To preserve mitochondrial integrity under diverse conditions, cells engage an interconnected network of mitochondrial quality control (MQC) mechanisms, namely mitochondrial biogenesis, maintenance of mitochondrial DNA (mtDNA), remodelling by fission and fusion, mitophagy, and the mitochondrial unfolded protein response. This review examines how these MQC systems govern macrophage polarization, inflammatory signalling, and survival in CVD, focusing on atherosclerosis, myocardial infarction, and heart failure. We discuss evidence demonstrating that the dysregulation of these mechanisms in macrophages, contributes to cardiovascular impairment, with particular emphasis on how dysregulated mitochondrial dynamics, heightened mitochondrial oxidative stress, and mtDNA release converge to amplify inflammation in CVD. We further highlight clinical evidence suggesting that current therapies, such as statins, SGLT2 inhibitors, and GLP-1 receptor agonists enhance macrophage MQC to alleviate stress, improve metabolic function, and dampen inflammation, which may contribute to their cardiovascular benefit. By examining the role of MQC in macrophages within the cardiovascular system, this review establishes the mechanisms governing mitochondrial homeostasis and dysfunction as a critical immunometabolic axis and potential therapeutic avenue underlying cardiovascular disease.

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Mitochondrial Quality Control in Macrophages during Cardiovascular Disease

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