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Targeting mitochondrial function in macrophages: A novel treatment strategy for atherosclerotic cardiovascular
Pierre-Hadrien Becker1, Patrice Thérond1, Pauline Gaignard1
1Université Paris-Saclay, EA 7357, Lipides: Systèmes Analytiques et Biologiques, Châtenay-Malabry 92296, France; Hôpital Bicêtre, AP-HP, Laboratoire de Biochimie, Le Kremlin Bicêtre 94270, France.
Insights
Mitochondrial dysfunction in macrophages drives atherosclerosis progression. Strategies to preserve macrophage mitochondrial function may offer new therapeutic avenues for treating atherosclerotic cardiovascular disease.
Area of Science:
- Cardiovascular Research
- Mitochondrial Biology
- Immunology
Background:
- Atherosclerotic cardiovascular disease (ASCVD) is a leading cause of death, driven by chronic arterial injury.
- Mitochondrial dysfunction and alterations in macrophages within atherosclerotic plaques are linked to disease progression.
- Macrophages play a crucial role in atherogenesis, with their functions dependent on mitochondrial metabolism.
Purpose of the Study:
- To review potential therapeutic strategies aimed at improving macrophage mitochondrial function.
- To explore how enhanced mitochondrial function can help macrophages maintain atheroprotective capacity.
- To discuss the role of emerging therapies in counteracting atherosclerotic lesion progression and promoting regression.
Main Methods:
- Review of recent scientific literature on mitochondrial dysfunction in atherosclerosis.
- Analysis of the role of macrophages and their mitochondrial metabolism in atherogenesis.
- Evaluation of in vitro studies on oxidized LDL effects on macrophage mitochondria.
Main Results:
- Mitochondrial dysfunction in macrophages contributes to inflammation and oxidative stress in ASCVD.
- Oxidized LDL impairs macrophage mitochondrial function, promoting a pro-inflammatory state.
- Preservation of mitochondrial function is a promising therapeutic target for ASCVD.
Conclusions:
- Maintaining macrophage mitochondrial health is critical for atheroprotective functions.
- Therapeutic strategies targeting mitochondrial function could prevent ASCVD progression.
- Improving macrophage mitochondrial capacity may lead to regression of atherosclerotic lesions.
Abstract:
Atherosclerotic cardiovascular disease is a major cause of morbidity and mortality due to chronic arterial injury caused by hyperlipidemia, hypertension, inflammation and oxidative stress. Recent studies have shown that the progression of this disease is associated with mitochondrial dysfunction and with the accumulation of mitochondrial alterations within macrophages of atherosclerotic plaques. These alterations contribute to processes of inflammation and oxidative stress. Among the many players involved, macrophages play a pivotal role in atherogenesis as they can exert both beneficial and deleterious effects due to their anti- and pro-inflammatory properties. Their atheroprotective functions, such as cholesterol efflux and efferocytosis, as well as the maintenance of their polarization towards an anti-inflammatory state, are particularly dependent on mitochondrial metabolism. Moreover, in vitro studies have demonstrated deleterious effects of oxidized LDL on macrophage mitochondrial function, resulting in a switch to a pro-inflammatory state and to a potential loss of atheroprotective capacity. Therefore, preservation of mitochondrial function is now considered a legitimate therapeutic strategy. This review focuses on the potential therapeutic strategies that could improve the mitochondrial function of macrophages, enabling them to maintain their atheroprotective capacity. These emerging therapies could play a valuable role in counteracting the progression of atherosclerotic lesions and possibly inducing their regression.
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