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      Sestrin2 as a Protective Shield against Cardiovascular Disease.

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          Abstract

          A timely and adequate response to stress is inherently present in each cell and is important for maintaining the proper functioning of the cell in changing intracellular and extracellular environments. Disruptions in the functioning or coordination of defense mechanisms against cellular stress can reduce the tolerance of cells to stress and lead to the development of various pathologies. Aging also reduces the effectiveness of these defense mechanisms and results in the accumulation of cellular lesions leading to senescence or death of the cells. Endothelial cells and cardiomyocytes are particularly exposed to changing environments. Pathologies related to metabolism and dynamics of caloric intake, hemodynamics, and oxygenation, such as diabetes, hypertension, and atherosclerosis, can overwhelm endothelial cells and cardiomyocytes with cellular stress to produce cardiovascular disease. The ability to cope with stress depends on the expression of endogenous stress-inducible molecules. Sestrin2 (SESN2) is an evolutionary conserved stress-inducible cytoprotective protein whose expression is increased in response to and defend against different types of cellular stress. SESN2 fights back the stress by increasing the supply of antioxidants, temporarily holding the stressful anabolic reactions, and increasing autophagy while maintaining the growth factor and insulin signaling. If the stress and the damage are beyond repair, SESN2 can serve as a safety valve to signal apoptosis. The expression of SESN2 decreases with age and its levels are associated with cardiovascular disease and many age-related pathologies. Maintaining sufficient levels or activity of SESN2 can in principle prevent the cardiovascular system from aging and disease.

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          Author and article information

          Journal
          Int J Mol Sci
          International journal of molecular sciences
          MDPI AG
          1422-0067
          1422-0067
          Mar 02 2023
          : 24
          : 5
          Affiliations
          [1 ] Department of Pharmaceutical Sciences, College of Pharmacy, QU Health, Qatar University, Doha P.O. Box 2713, Qatar.
          [2 ] Department of Social Sciences, College of Arts and Sciences, Qatar University, Doha P.O. Box 2713, Qatar.
          [3 ] The Neuroscience Institute, Academic Health System, Hamad Medical Corporation (HMC), Doha P.O. Box 3050, Qatar.
          [4 ] Department of Basic Medical Science, College of Medicine, QU health, Qatar University, Doha P.O. Box 2713, Qatar.
          [5 ] Biomedical Research Center (BRC), Qatar University, Doha P.O. Box 2713, Qatar.
          [6 ] Office of Vice President for Research and Graduate Studies, Qatar University, Doha P.O. Box 2713, Qatar.
          Article
          ijms24054880
          10.3390/ijms24054880
          10003517
          36902310
          0374db23-e7f8-4459-b070-c6c0a1eaaf94
          History

          Sestrin2,oxidative stress,cellular stress,cardiovascular disease,cardioprotective,antioxidant

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