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      Basic Biology of Oxidative Stress and the Cardiovascular System: Part 1 of 3-Part Series

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          Abstract

          The generation of reactive oxygen species (ROS) is a fundamental aspect of normal human biology. However, when ROS generation exceeds endogenous antioxidant capacity, oxidative stress arises. If unchecked, ROS production and oxidative stress mediate tissue and cell damage that can spiral in a cycle of inflammation and more oxidative stress. This article is Part 1 of a 3-part series covering The Role of Oxidative Stress in Cardiovascular Disease. The broad theme of this first paper is the mechanisms and biology of oxidative stress. Specifically, we review the basic biology of oxidative stress, relevant aspects of mitochondrial function, and stress-related cell death pathways (apoptosis and necrosis) as they relate to the heart and cardiovascular system. We then explore telomere biology and cell senescence. As important regulators and sensors of oxidative stress, telomeres are segments of repetitive nucleotide sequence at each end of a chromosome that protect the chromosome ends from deterioration.

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          Author and article information

          Journal
          8301365
          4429
          J Am Coll Cardiol
          J. Am. Coll. Cardiol.
          Journal of the American College of Cardiology
          0735-1097
          1558-3597
          20 June 2017
          11 July 2017
          11 July 2018
          : 70
          : 2
          : 196-211
          Affiliations
          [a ]Cardiovascular and Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland
          [b ]Minerva Institute for Medical Research, Helsinki, Finland
          [c ]The Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, New York
          [d ]Marie-Josée and Henry R. Kravis Cardiovascular Health Center, Icahn School of Medicine at Mount Sinai, New York, New York
          [e ]Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain
          Author notes
          Address for Correspondence: Dr. Jason Kovacic, Cardiovascular Institute, Mount Sinai Hospital, One Gustave L. Levy Place, Box 1030, New York, New York 10029, Telephone: 646.593.2552, Fax: 212-534-2845, jason.kovacic@ 123456mountsinai.org , Dr. Michael N. Sack, Cardiovascular and Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Building 10-CRCm, Room 5-3150, 10 Center Drive, Bethesda, Maryland 20892-1454, Telephone: Tel: 301-402-9259, Fax: 301-402-0888, sackm@ 123456nih.gov , Dr. Frej Y. Fyhrquist, Minerva Institute for Medical Research, Biomedicum U2, Haartmaninkatu 8, 00290 Helsinki, Finland, Telephone: 358 0 8410004, Fax: frej.fyhrquist@ 123456helsinki.fi

          Drs. Sack, Fyhrquist, and Saijonmaa contributed equally to this work.

          Article
          PMC5551687 PMC5551687 5551687 nihpa885808
          10.1016/j.jacc.2017.05.034
          5551687
          28683968
          59b13695-d5c8-41e2-9b25-7cf03de805be
          History
          Categories
          Article

          apoptosis,mitochondria,necrosis,reactive oxygen species,senescence,sirtuin,telomere

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