作者: David I. Brown , Traci L. Parry , Monte S. Willis
DOI: 10.1002/CPHY.C160024
关键词:
摘要: Heart failure (HF) is a costly and deadly syndrome characterized by the reduced capacity of heart to adequately provide systemic blood flow. Mounting evidence implicates pathological changes in cardiac energy metabolism as contributing factor development HF. While main source fuel healthy oxidation fatty acids, failing less efficient glucose glycogen are upregulated. The ubiquitin proteasome system plays key role regulating via protein-degradation/regulation autophagy metabolism-related transcription cell signaling processes. In this review, we discuss recent research that describes ubiquitin-proteasome (UPS) context We focus on ligases (E3s), component UPS confers substrate specificity, detail current understanding how these E3s contribute pathology metabolism. © 2017 American Physiological Society. Compr Physiol 7:841-862, 2017.