Redox Biology of Right-Sided Heart Failure

被引:14
|
作者
Shults, Nataliia V. [1 ]
Melnyk, Oleksiy [1 ]
Suzuki, Dante I. [1 ]
Suzuki, Yuichiro J. [1 ]
机构
[1] Georgetown Univ, Med Ctr, Dept Pharmacol & Physiol, 3900 Reservoir Rd NW, Washington, DC 20007 USA
来源
ANTIOXIDANTS | 2018年 / 7卷 / 08期
关键词
antioxidants; redox; reactive oxygen species; right heart failure; RIGHT VENTRICLE; PULMONARY-HYPERTENSION; PROTEIN CARBONYLATION; MOLECULAR-MECHANISMS; TRANSCRIPTION FACTOR; CARDIAC-HYPERTROPHY; OXIDATIVE STRESS; GATA4; PHOSPHORYLATION; ASSOCIATION;
D O I
10.3390/antiox7080106
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Right-sided heart failure is the major cause of death among patients who suffer from various forms of pulmonary hypertension and congenital heart disease. The right ventricle (RV) and left ventricle (LV) originate from different progenitor cells and function against very different blood pressures. However, differences between the RV and LV formed after birth have not been well defined. Work from our laboratory and others has accumulated evidence that redox signaling, oxidative stress and antioxidant regulation are important components that define the RV/LV differences. The present article summarizes the progress in understanding the roles of redox biology in the RV chamber-specificity. Understanding the mechanisms of RV/LV differences should help develop selective therapeutic strategies to help patients who are susceptible to and suffering from right-sided heart failure. Modulations of redox biology may provide effective therapeutic avenues for these conditions.
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页数:9
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