Genetically induced moderate inhibition of 20S proteasomes in cardiomyocytes facilitates heart failure in mice during systolic overload

• Published in: Journal of molecular and cellular cardiology Vol. 85; pp. 273 - 281
• Main Authors: Ranek, Mark J., Zheng, Hanqiao, Huang, Wei, Kumarapeli, Asangi R., Li, Jie, Liu, Jinbao, Wang, Xuejun
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.08.2015
• Subjects: Animals; Aortic Diseases - complications; Aortic Diseases - enzymology; Cardiac hypertrophy; Cardiomegaly - enzymology; Cardiomegaly - etiology; Cardiovascular; Heart Failure; Heart Ventricles - enzymology; Heart Ventricles - pathology; Mice, Transgenic; Myocytes, Cardiac - enzymology; Pressure overload; Proteasome Endopeptidase Complex - genetics; Proteasome inhibition; Proteolysis; Transgenic mice; Ubiquitination; Ubiquitin–proteasome system; Ventricular Pressure; CHF; NTG; Heart failure; PQC; Transgenic mice; Cardiac hypertrophy; Pressure overload; LV; Ubiquitin–proteasome system; CR-PsmI; PFI; TG; Proteasome inhibition; TAC; PsmI; UPS; proteasome functional insufficiency; left ventricle; ubiquitin–proteasome system; cardiomyocyte-restricted PsmI; proteasome inhibition; protein quality control; transverse aortic constriction; congestive heart failure; transgenic; non-transgenic

The in vivo function status of the ubiquitin–proteasome system (UPS) in pressure overloaded hearts remains undefined. Cardiotoxicity was observed during proteasome inhibitor chemotherapy, especially in those with preexisting cardiovascular conditions; however, proteasome inhibition (PsmI) was also s...