Journalartikel

Review on Chamber-Specific Differences in Right and Left Heart Reactive Oxygen Species Handling


AutorenlisteSchlueter, Klaus-Dieter; Kutsche, Hanna Sarah; Hirschhaeuser, Christine; Schreckenberg, Rolf; Schulz, Rainer

Jahr der Veröffentlichung2018

ZeitschriftFrontiers in Physiology

Bandnummer9

ISSN1664-042X

Open Access StatusGold

DOI Linkhttps://doi.org/10.3389/fphys.2018.01799

VerlagFrontiers 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.



Zitierstile

Harvard-ZitierstilSchlueter, 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-ZitierstilSchlueter, 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



Schlagwörter


ANGIOTENSIN-IIcardiac remodelingINDUCED CARDIAC-HYPERTROPHYMAOMYOCARDIAL OXIDATIVE STRESSNADPH OXIDASENITRIC-OXIDE SYNTHASEPRESSURE-OVERLOADPULMONARY ARTERIAL-HYPERTENSIONPulmonary hypertensionRIGHT-VENTRICULAR HYPERTROPHYSUPEROXIDE-DISMUTASEuncoupling protein


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