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Published on: November 17, 2017
Role of Mammalian Target of Rapamycin in Atherosclerosis
1Department of Neurology, Chongqing General Hospital, University of Chinese Academy of Sciences, 400013, Chongqing, China.
Abstract:
The mammalian target of rapamycin (mTOR) regulates multiple pathophysiological processes, such as cell development, angiogenesis, autophagy, as well as innate-adaptive immune responses. Numerous studies have demonstrated that mTOR signaling plays an important role in the process of atherosclerosis (AS) itself or AS-related diseases. The activation of mTOR signaling contributes to the endothelium dysfunction and the formation of foam cells via enhancing the process from monocyte to macrophage in the initial stage of atherosclerosis. The activation of mTOR signaling not only promotes the formation of the fatty streak (more foam cells), and migration and proliferation of vascular smooth muscle cells in the early lesion of AS, but also facilitates the formation of vulnerable plaque and replication of vascular smooth muscle cells in the late lesion of AS. Moreover, it has been found the role of the upstream and downstream components of mTOR signaling pathway in the formation of AS. Thus, the mTOR inhibitors may be a promising target for the prevention and treatment of AS.
Insights
The mammalian target of rapamycin (mTOR) pathway is crucial in atherosclerosis development. Inhibiting mTOR may offer a promising therapeutic strategy for preventing and treating this cardiovascular disease.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Immunology
Background:
- The mammalian target of rapamycin (mTOR) signaling pathway regulates critical cellular functions including immune responses.
- mTOR signaling is implicated in various pathophysiological processes, including atherosclerosis (AS).
Purpose of the Study:
- To elucidate the role of mTOR signaling in the pathogenesis of atherosclerosis.
- To evaluate the potential of mTOR inhibitors as therapeutic agents for AS.
Main Methods:
- Review of existing literature on mTOR signaling and atherosclerosis.
- Analysis of the involvement of mTOR pathway components in AS development.
Main Results:
- mTOR activation contributes to endothelial dysfunction and foam cell formation in early AS.
- Activated mTOR promotes fatty streak formation, vascular smooth muscle cell migration, proliferation, and vulnerable plaque development in AS lesions.
- Upstream and downstream components of the mTOR pathway are involved in AS formation.
Conclusions:
- mTOR signaling is a key driver in both early and late stages of atherosclerosis.
- Targeting mTOR with inhibitors presents a promising therapeutic avenue for AS prevention and treatment.
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