Author + information
- Received January 16, 2017
- Revision received April 25, 2017
- Accepted May 10, 2017
- Published online July 3, 2017.
- Bernd Niemann, MDa,
- Susanne Rohrbach, MDb,∗∗ (, )
- Mark R. Miller, PhDc,
- David E. Newby, MDc,∗∗∗ (, )
- Valentin Fuster, MD, PhDd,e,f and
- Jason C. Kovacic, MD, PhDd,∗ ()
- aDepartment of Adult and Pediatric Cardiovascular Surgery, University Hospital Giessen, Giessen, Germany
- bInstitute of Physiology, Justus-Liebig University, Giessen, Germany
- cBHF/University of Edinburgh Centre for Cardiovascular Science, The Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom
- dThe Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, New York
- eMarie-Josée and Henry R. Kravis Cardiovascular Health Center, Icahn School of Medicine at Mount Sinai, New York, New York
- fCentro Nacional de Investigaciones Cardiovasculares, Madrid, Spain
- ↵∗Address for correspondence:
Dr. Jason C. Kovacic, Cardiovascular Institute, Mount Sinai Hospital, One Gustave L. Levy Place, Box 1030, New York, New York 10029.
- ↵∗∗Dr. Susanne Rohrbach, Institute of Physiology, Justus-Liebig University Giessen, Aulweg 129, 35392 Giessen, Germany.
- ↵∗∗∗Prof. David E. Newby, BHF Centre for Cardiovascular Science, University of Edinburgh, Chancellor's Building, 49 Little France Crescent, Little France, Edinburgh, United Kingdom, EH16 4SB.
Oxidative stress occurs whenever the release of reactive oxygen species (ROS) exceeds endogenous antioxidant capacity. In this paper, we review the specific role of several cardiovascular risk factors in promoting oxidative stress: diabetes, obesity, smoking, and excessive pollution. Specifically, the risk of developing heart failure is higher in patients with diabetes or obesity, even with optimal medical treatment, and the increased release of ROS from cardiac mitochondria and other sources likely contributes to the development of cardiac dysfunction in this setting. Here, we explore the role of different ROS sources arising in obesity and diabetes, and the effect of excessive ROS production on the development of cardiac lipotoxicity. In parallel, contaminants in the air that we breathe pose a significant threat to human health. This paper provides an overview of cigarette smoke and urban air pollution, considering how their composition and biological effects have detrimental effects on cardiovascular health.
- air pollution
- metabolic stress
- particulate matter
Dr. Rohrbach has received research support from the German Research Foundation (IRTG1566, SFB1213). Drs. Miller and Newby have received funding from grants (PG/10/042/28388, RG/10/9/28286, FS/10/024/28266, SP/15/8/31575, and FS/16/14/32023) and chair (CH/09/002) awards from the British Heart Foundation. Dr. Kovacic has received research support from the National Institutes of Health (R01HL130423), the American Heart Association (14SFRN20490315 and 14SFRN20840000), and The Leducq Foundation (Transatlantic Network of Excellence Award). All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Drs. Niemann, Rohrbach, Miller, and Newby contributed equally to this work. Kathy Griendling, PhD, served as Guest Editor for this paper.
- Received January 16, 2017.
- Revision received April 25, 2017.
- Accepted May 10, 2017.
- 2017 American College of Cardiology Foundation