作者: Ruijie Liu , Jeffery D. Molkentin
DOI: 10.1016/J.YJMCC.2016.08.018
关键词:
摘要: Mitogen-activated protein kinases (MAPKs) play a critical role in regulating cardiac hypertrophy and remodeling response to increased workload or pathological insults. The spatiotemporal activities inactivation of MAPKs are tightly controlled by family dual-specificity MAPK phosphatases (DUSPs). Over the past 2 decades, we others have determined for selected DUSP members controlling activity heart ensuing effects on ventricular growth remodeling. More specifically, studies from mice deficient individual Dusp genes as well heart-specific inducible transgene-mediated overexpression implicated select DUSPs essential signaling effectors that function dynamically level, subcellular temporal extracellular signal-regulated (ERKs), c-Jun N-terminal (JNKs) p38 MAPKs. This review summarizes recent literature physiological roles MAPK-specific effect