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Macrophage mitochondrial superoxides as a target for atherosclerotic disease treatment
Laszlo A Groh1, Niels P Riksen1
1Department of Internal Medicine & Radboud Institute of Molecular Life Sciences (RIMLS), Radboud University Medical Center, Nijmegen, the Netherlands.
Insights
This review explores targeting mitochondrial superoxides in monocytes to treat cardiovascular diseases (CVD). Strategies aim to reduce inflammation and improve therapies for atherosclerosis, a major cause of CVD.
Area of Science:
- Cardiovascular research
- Immunology
- Mitochondrial metabolism
Background:
- Cardiovascular diseases (CVD) are the leading global cause of mortality.
- Existing therapies inadequately protect a significant patient population.
- Inflammation is a key driver in atherosclerosis, the underlying cause of many CVDs.
Purpose of the Study:
- To review strategies for lowering mitochondrial superoxides in monocytes.
- To explore targeted therapies for monocytes and macrophages in atherosclerosis.
- To enhance treatment efficacy and minimize side effects for cardiovascular disease.
Main Methods:
- Review of current literature on inflammation in atherosclerosis.
- Analysis of the role of mitochondrial metabolism and superoxides in monocytes.
- Exploration of therapeutic strategies targeting monocytes and macrophages.
Main Results:
- Monocytes exhibit increased mitochondrial metabolism and superoxide production in atherosclerosis.
- A link exists between mitochondrial superoxides and inflammatory responses in monocytes.
- Targeting these pathways offers potential for novel CVD treatments.
Conclusions:
- Lowering mitochondrial superoxides presents a promising therapeutic avenue for CVD.
- Selective targeting of monocytes/macrophages can improve treatment outcomes.
- Further research into these strategies may broaden CVD treatment options.
Abstract:
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.
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