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Published on: June 3, 2014
Sestrin2 in atherosclerosis
Zhen Tian1, Bin-Jie Yan1, Wen Luo1
1Institute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan Province, International Joint Laboratory for Arteriosclerotic Disease Research of Hunan Province, University of South China, Hengyang 421001, China.
Abstract:
Atherosclerosis (AS) is the pathological basis of numerous lethal diseases, such as myocardial infarction, heart failure, and stroke. As we know, almost twenty million people worldwide die of the arterial diseases annually. Sestrin2 is a stress-inducing protein, which serves as a guardian by activating AMPK, inhibiting mTOR, and maintaining redox balance beneath various stress environments. A large number of studies show that Sestrin2 would shield the body from injury by stress. Moreover, it has been demonstrated that Sestrin2 is closely connected with AS. Here, this article reviewed the involvement of Sestrin2 in the pathogenesis of AS from four aspects: cellular mechanism, oxidative stress, inflammation, and lipid metabolism. Current evidence reveals that Sestrin2 is a novel target for the prevention and treatment of AS.
Insights
Sestrin2 protein protects against atherosclerosis (AS), a major cause of heart disease and stroke. This review highlights Sestrin2
Area of Science:
- Biochemistry and Molecular Biology
- Cardiovascular Research
- Pathophysiology
Background:
- Atherosclerosis (AS) is a primary pathological process underlying major lethal cardiovascular diseases, including myocardial infarction, heart failure, and stroke.
- Millions of deaths worldwide are attributed annually to arterial diseases, underscoring the urgent need for effective therapeutic strategies.
- Sestrin2, a stress-inducible protein, plays a crucial role in cellular protection by activating AMPK, inhibiting mTOR, and maintaining redox balance under stress.
Purpose of the Study:
- To review the multifaceted involvement of Sestrin2 in the pathogenesis of atherosclerosis.
- To explore the role of Sestrin2 in cellular mechanisms, oxidative stress, inflammation, and lipid metabolism relevant to AS.
- To evaluate Sestrin2 as a potential therapeutic target for AS prevention and treatment.
Main Methods:
- Literature review synthesizing current evidence on Sestrin2's function in stress response and cellular pathways.
- Analysis of studies investigating the correlation between Sestrin2 expression/activity and the development of atherosclerosis.
- Examination of Sestrin2's impact on key pathological hallmarks of AS, including oxidative stress, inflammation, and lipid dysregulation.
Main Results:
- Sestrin2 exhibits protective effects against cellular injury induced by various stress conditions.
- Evidence strongly links Sestrin2 to the pathogenesis of atherosclerosis through modulation of cellular mechanisms, oxidative stress, inflammation, and lipid metabolism.
- Sestrin2 activation of AMPK and inhibition of mTOR pathways are key mechanisms contributing to its atheroprotective effects.
Conclusions:
- Sestrin2 plays a significant role in protecting against the development and progression of atherosclerosis.
- The multifaceted functions of Sestrin2 in cellular defense and metabolic regulation make it a promising therapeutic target.
- Targeting Sestrin2 offers a novel strategy for the prevention and treatment of atherosclerosis and related cardiovascular diseases.
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