Open Accessndufa7 plays a critical role in cardiac hypertrophy
Author(s) -
Shi Xingjuan,
Zhang Yu,
Chen Ru,
Gong Yijie,
Zhang Mingming,
Guan Rui,
Rotstein Ori D.,
Liu Xiangdong,
Wen XiaoYan
Publication year - 2020
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.15921
Subject(s) - muscle hypertrophy , hypertrophic cardiomyopathy , medicine , heart failure , zebrafish , dilated cardiomyopathy , pathological , calcineurin , cardiomyopathy , cardiac function curve , cardiology , gene knockdown , myocyte , endocrinology , biology , gene , transplantation , genetics
Cardiac hypertrophy is a common pathological change in patients with progressive cardiac function failure, which can be caused by hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy (DCM) or arterial hypertension. Despite years of study, there is still limited knowledge about the underlying molecular mechanisms for cardiac hypertrophy. NDUFA7, a subunit of NADH:ubiquinone oxidoreductase (complex I), has been reported to be a novel HCM associated gene. However, the biological role of NDUFA7 in heart remains unknown. In this study, we found that NDUFA7 exhibited high expression in the heart, and its level was significantly decreased in mice model of cardiac hypertrophy. Moreover, we demonstrated that ndufa7 knockdown in developing zebrafish embryos resulted in cardiac development and functional defects, associated with increased expression of pathological hypertrophy biomarkers nppa (ANP) and nppb (BNP). Mechanistic study demonstrated that ndufa7 depletion promoted ROS production and calcineurin signalling activation. Moreover, NDUFA7 depletion contributed to cardiac cell hypertrophy. Together, these results report for the first time that ndufa7 is implicated in pathological cardiac hypertrophy.