Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
, 9, 1799
eCollection

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

Affiliations

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

Klaus-Dieter Schlüter et al. Front Physiol.

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.

Keywords: MAO; cardiac remodeling; heart failure; oxidative stress; pulmonary hypertension; uncoupling protein.

Figures

Figure 1
Figure 1
Sources of reactive oxygen species in cardiomyocytes. (A) Complex I and III of the electron transport chain (ETC) constitutively release O2.- and complex II can be activated by NOX-dependent ROS. (B) Monoamine oxidase (MAO) generates H2O2. (C) Xanthine oxidase (XO) catalyzes a two-step reaction leading to additional release of H2O2. (D) Uncoupling of nitric oxide synthase (NOS) leads to generation of O2.-. (E) NADPH oxidase (NOX) generates also O2.- upon activation.
Figure 2
Figure 2
ROS defense systems in cardiomyocytes. (A) Superoxide dismutases catalyze the formation of H2O2 that can be detoxificated by catalase (B). (C) Gluatathione peroxidase (GPX) reduces H2O2. (D) Coupled NOS generates NO that neutralizes O2.-.
Figure 3
Figure 3
Differences between right (RV) and left (LV) ventricular cardiomyocytes. LV cardiomyocytes are longer (A), wider (B), larger (C), less mono-nucleated (D), have a reduced cell spreading (E) as adaptation to culture conditions, and a stronger load-free cell shortening (F). Furthermore, mitochondria from RV generate more ROS (G). Data depicted from Schreckenberg et al. (2015) and Schlüter (2016). *p < 0.05 vs. LV.

Similar articles

See all similar articles

Cited by 5 articles

References

    1. Abraham W. T., Raynolds M. V., Badesch D. B., Wynne K. M., Groves B. M., Roden R. L., et al. . (2003). Angiotensin-converting enzyme DD genotype in patients with primary pulmonary hypertension: increased frequency and association with preserved haemodynamics. J. Renin. Angiot. Aldoster. Syst. 4, 27–30. 10.3317/jraas.2003.003 - DOI - PubMed
    1. Adesina S. E., Wade B. E., Bijli K. M., Kang B. Y., Williams C. R., Ma J., et al. . (2017). Hypoxia inhibits expression and function of mitochondrial thioredoxin 2 to promote pulmonary hypertension. Am. J. Physiol. Lung Cell. Mol. Physiol. 312, L599–L608. 10.1152/ajplung.00258.2016 - DOI - PMC - PubMed
    1. Alzoubi A., Toba M., Abe K., O'Neill K. D., Rocic P., Fagan K. A., et al. . (2013). Dehydroepiandrosterone restores right ventricular structure and function in rats with severe pulmonary arterial hypertension. Am. J. Physiol. Heart Circ. Physiol. 304, H1708–H1718. 10.1152/ajpheart.00746.2012 - DOI - PubMed
    1. Ameri P., Bertero E., Meliota G., Cheli M., Canepa M., Brunelli C., et al. . (2016). Neurohormonal activation and pharmacological inhibition in pulmonary arterial hypertension and related right ventricular failure. Heart Fail. Rev. 21, 539–547. 10.1007/s10741-016-9566-3 - DOI - PubMed
    1. Anghel N., Herman H., Balta C., Rosu M., Stan M. S., Nita D., et al. . (2018). Acute cardiotoxicity induced by doxorubicin in right ventricle is associated with increase of oxidative stress and apoptosis in rats. Histol. Histopathol. 33, 365–378. 10.14670/HH-11-932 - DOI - PubMed

LinkOut - more resources

Feedback