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      SIRT3: A New Regulator of Cardiovascular Diseases

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          Abstract

          Cardiovascular diseases (CVDs) are the leading causes of death worldwide, and defects in mitochondrial function contribute largely to the occurrence of CVDs. Recent studies suggest that sirtuin 3 (SIRT3), the mitochondrial NAD +-dependent deacetylase, may regulate mitochondrial function and biosynthetic pathways such as glucose and fatty acid metabolism and the tricarboxylic acid (TCA) cycle, oxidative stress, and apoptosis by reversible protein lysine deacetylation. SIRT3 regulates glucose and lipid metabolism and maintains myocardial ATP levels, which protects the heart from metabolic disturbances. SIRT3 can also protect cardiomyocytes from oxidative stress-mediated cell damage and block the development of cardiac hypertrophy. Recent reports show that SIRT3 is involved in the protection of several heart diseases. This review discusses the progress in SIRT3-related research and the role of SIRT3 in the prevention and treatment of CVDs.

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          Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study

          Mahshid Dehghan, Andrew Mente, Xiaohe Zhang … (2017)
          The relationship between macronutrients and cardiovascular disease and mortality is controversial. Most available data are from European and North American populations where nutrition excess is more likely, so their applicability to other populations is unclear.
          Article 0 comments Cited 379 times – based on 0 reviews     Review now
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            Nutrient-sensitive mitochondrial NAD+ levels dictate cell survival.

            Hongying Yang, Tianle Yang, Joseph A. Baur … (2007)
            A major cause of cell death caused by genotoxic stress is thought to be due to the depletion of NAD(+) from the nucleus and the cytoplasm. Here we show that NAD(+) levels in mitochondria remain at physiological levels following genotoxic stress and can maintain cell viability even when nuclear and cytoplasmic pools of NAD(+) are depleted. Rodents fasted for 48 hr show increased levels of the NAD(+) biosynthetic enzyme Nampt and a concomitant increase in mitochondrial NAD(+). Increased Nampt provides protection against cell death and requires an intact mitochondrial NAD(+) salvage pathway as well as the mitochondrial NAD(+)-dependent deacetylases SIRT3 and SIRT4. We discuss the relevance of these findings to understanding how nutrition modulates physiology and to the evolution of apoptosis.
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              Hypertrophy of the heart: a new therapeutic target?

              Norbert Frey, Hugo Katus, Eric Olson … (2004)
              Recent studies call into question the necessity of hypertrophic growth of the heart as a "compensatory" response to hemodynamic stress. These findings, coupled with recent progress in dissecting the molecular bases of hypertrophy, raise the prospect of suppressing hypertrophy without provoking circulatory insufficiency. In this article, we focus on signaling pathways that hold promise as potential targets for therapeutic intervention. We also summarize observations from animal models and clinical trials that suggest benefit from an antihypertrophic strategy.
              Article 0 comments Cited 208 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Bin Liu:
                ORCID: http://orcid.org/0000-0003-2017-2160
                Journal
                Journal ID (nlm-ta): Oxid Med Cell Longev
                Journal ID (iso-abbrev): Oxid Med Cell Longev
                Journal ID (publisher-id): OMCL
                Title: Oxidative Medicine and Cellular Longevity
                Publisher: Hindawi
                ISSN (Print): 1942-0900
                ISSN (Electronic): 1942-0994
                Publication date Collection: 2018
                Publication date (Electronic): 13 February 2018
                Volume: 2018
                Electronic Location Identifier: 7293861
                Affiliations
                1Department of Cardiology, The Second Hospital of Jilin University, 218 Ziqiang Road, Changchun 130041, China
                2Department of Neurology, The Liaoning Province People's Hospital, 33 Wenyi Road, Shenyang 110016, China
                3Department of Neurology, The Second Hospital of Jilin University, 218 Ziqiang Road, Changchun 130041, China
                Author notes

                Academic Editor: Ada Popolo

                Author information
                http://orcid.org/0000-0003-2017-2160
                Article
                DOI: 10.1155/2018/7293861
                PMC ID: 5831850
                PubMed ID: 29643974
                SO-VID: 06c67f33-3b4f-4faf-b8ba-df25ac0626b6
                Copyright © Copyright © 2018 Wei Sun et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 1 November 2017
                Date revision received : 20 December 2017
                Date accepted : 4 January 2018
                Funding
                Funded by: National Clinical Key Specialty Project
                Funded by: Ph.D. Outstanding Personnel Development Program of Bethune Medical Department
                Award ID: yb201503
                Funded by: National Natural Science Foundation of China
                Award ID: 81570250
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Molecular medicine
                Data availability:
                ScienceOpen disciplines: Molecular medicine

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