Degradation systems in heart failure. (July 2015)

• Record Type: Journal Article
• Authors: Nishida, Kazuhiko; Yamaguchi, Osamu; Otsu, Kinya
• Is Part Of: Journal of molecular and cellular cardiology. Volume 84(2015:Jul.)
• Page Start: 212
• Page End: 222
• Publication Date: 2015-07
• Subjects: AMPK AMP-activated protein kinase -- ASK1 apoptosis signal-regulating kinase 1 -- Atg autophagy-related -- ARE AU-rich element -- AUF ARE RNA binding protein -- BRF butyrate response factor -- CaMK Ca2 +/calmodulin-dependent protein kinase -- CUGBP CUG-binding protein -- CryAB αB-crystallin -- DRC desmin-related cardiomyopathy -- DNase deoxyribonuclease -- GPCR G protein-coupled receptor -- HuR Hu-antigen R -- IκB inhibitor of NF-κB -- IKK IκB kinase -- KSRP KH-type splicing regulatory protein -- IL interleukin -- I/R ischemia/reperfusion -- LAMP2 lysosome-associated membrane protein 2 -- MAP mitogen-activated protein -- MG53 mitsugumin 53 -- miRNA microRNA -- MK2 MAP kinase-activated protein kinase 2 -- mtDNA mitochondrial DNA -- NEMO NF-κB essential modulator -- NF-κB nuclear factor-κB -- Regnase-1 regulatory RNase 1 -- ROS reactive oxygen species -- SLE systemic lupus erythematosus -- STAT6 signal transducer and activator of transcription 6 -- TAC thoracic transverse aortic constriction -- TLR Toll-like receptor -- TNF tumor necrosis factor -- Trex1 three prime repair exonuclease 1 -- TTP tristetraprolin -- UTR untranslated region; Heart failure -- Calpain -- Autophagy -- Ubiquitin proteasome system -- Inflammation; Cardiology -- Periodicals; Heart Diseases -- Periodicals; Molecular Biology -- Periodicals; Cardiologie -- Périodiques; Cardiology; Electronic journals; Periodicals; 616.12
• DOI: 10.1016/j.yjmcc.2015.05.004
• Languages: English
• ISSNs: 0022-2828

Abstract

Abstract: Heart failure is a complex clinical syndrome that results from any structural or functional impairment of ventricular filling or the ejection of blood, and is a leading cause of morbidity and mortality in industrialized countries. The mechanisms underlying the development of heart failure are multiple, complex and not well understood. Cardiac mass and its homeostasis are maintained by the balance between protein synthesis and degradation, and an imbalance is likely to result in cellular dysfunction and disease. The protein degradation systems are the principle mechanisms for maintaining cellular homeostasis via protein quality control. Three major protein degradation systems have been identified, namely the calpain system, autophagy, and the ubiquitin proteasome system. Proinflammatory mediators involve the development and progression of heart failure. DNA and RNA degradation systems play a critical role in regulating inflammation and maintaining cellular homeostasis mediated by damaged DNA clearance and posttranscriptional regulation, respectively. This review discusses some recent advances in understanding the role of these degradation systems in heart failure. Highlights: The protein degradation systems maintain cellular homeostasis. Calpains are required for plasma membrane maintenance. Autophagy is a cardioprotective mechanism against external stress. DNA and RNA degradation systems regulate inflammation. Mitochondrial DNA that escapes from autophagy causes inflammation and heart failure.