Journal
CELLULAR SIGNALLING
Volume 84, Issue -, Pages -Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2021.110033
Keywords
Cardiac hypertrophy; Dual specificity phosphatases; Mitogen activated protein kinases
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Funding
- Rappaport Family Institute for Research in the Medical Sciences
- Israel Science Foundation [1385/20]
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Pressure overload and other stress stimuli lead to cardiac hypertrophy and heart failure through signaling cascades, with MAPK pathway and DUSPs playing important roles.
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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