Journal article
Authors list: Schlueter, Klaus-Dieter; Kutsche, Hanna Sarah; Hirschhaeuser, Christine; Schreckenberg, Rolf; Schulz, Rainer
Publication year: 2018
Journal: Frontiers in Physiology
Volume number: 9
ISSN: 1664-042X
Open access status: Gold
DOI Link: https://doi.org/10.3389/fphys.2018.01799
Publisher: Frontiers Media
Abstract:
Reactive oxygen species (ROS) exert signaling character (redox signaling), or damaging character (oxidative stress) on cardiac tissue depending on their concentration and/ or reactivity. The steady state of ROS concentration is determined by the interplay between its production (mitochondrial, cytosolic, and sarcolemmal enzymes) and ROS defense enzymes (mitochondria, cytosol). Recent studies suggest that ROS regulation is different in the left and right ventricle of the heart, specifically by a different activity of superoxide dismutase (SOD). Mitochondrial ROS defense seems to be lower in right ventricular tissue compared to left ventricular tissue. In this review we summarize the current evidence for heart chamber specific differences in ROS regulation that may play a major role in an observed inability of the right ventricle to compensate for cardiac stress such as pulmonary hypertension. Based on the current knowledge regimes to increase ROS defense in right ventricular tissue should be in the focus for the development of future therapies concerning right heart failure.
Citation Styles
Harvard Citation style: Schlueter, K., Kutsche, H., Hirschhaeuser, C., Schreckenberg, R. and Schulz, R. (2018) Review on Chamber-Specific Differences in Right and Left Heart Reactive Oxygen Species Handling, Frontiers in Physiology, 9, Article 1799. https://doi.org/10.3389/fphys.2018.01799
APA Citation style: Schlueter, K., Kutsche, H., Hirschhaeuser, C., Schreckenberg, R., & Schulz, R. (2018). Review on Chamber-Specific Differences in Right and Left Heart Reactive Oxygen Species Handling. Frontiers in Physiology. 9, Article 1799. https://doi.org/10.3389/fphys.2018.01799
Keywords
ANGIOTENSIN-II; cardiac remodeling; INDUCED CARDIAC-HYPERTROPHY; MAO; MYOCARDIAL OXIDATIVE STRESS; NADPH OXIDASE; NITRIC-OXIDE SYNTHASE; PRESSURE-OVERLOAD; PULMONARY ARTERIAL-HYPERTENSION; Pulmonary hypertension; RIGHT-VENTRICULAR HYPERTROPHY; SUPEROXIDE-DISMUTASE; uncoupling protein