Dual specific phosphatases (DUSPs) in cardiac hypertrophy and failure |
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| Institution: | 1. Central Texas Veterans Health Care System, College of Medicine, Texas A&M Health Science Center, 1901 South 1st Street, Temple, TX 76504, United States;2. Department of Medical Physiology, Cardiovascular Research Institute, College of Medicine, Texas A&M Health Science Center, 1901 South 1st Street, Temple, TX 76504, United States;3. Division of Gastroenterology, College of Medicine, Texas A&M Health Science Center, 1901 South 1st Street, Temple, TX 76504, United States;1. Department of Cardiology, The First College of Clinical Medical Science, China Three Gorges University, Yichang 443000, China;2. Institute of Cardiovascular Diseases, China Three Gorges University, Yichang 443000, China;3. Central Laboratory, Yichang Central People''s Hospital, Yichang 443000, China;1. Department of Pharmacology, University of Minnesota, MN 55455, USA;2. Department of Integrative Biology and Physiology, University of Minnesota, MN 55455, USA |
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| Abstract: | Pressure overload and other stress stimuli elicit a host of adaptive and maladaptive signaling cascades that eventually lead to cardiac hypertrophy and heart failure. Among those, the mitogen-activated protein kinase (MAPK) signaling pathway has been shown to play a prominent role. The dual specificity phosphatases (DUSPs), also known as MAPK specific phosphatases (MKPs), that can dephosphorylate the MAPKs and inactivate them are gaining increasing attention as potential drug targets. Here we try to review recent advancements in understanding the roles of the different DUSPs, and the pathways that they regulate in cardiac remodeling. We focus on the regulation of three main MAPK branches – the p38 kinases, the c-Jun-N-terminal kinases (JNKs) and the extracellular signal-regulated kinases (ERK) by various DUSPs and try to examine their roles. |
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