Dual specific phosphatases (DUSPs) in cardiac hypertrophy and failure

Michael Mutlak, Izhak Kehat

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Article number110033
JournalCellular Signalling
StatePublished - Aug 2021


  • Cardiac hypertrophy
  • Dual specificity phosphatases
  • Mitogen activated protein kinases

All Science Journal Classification (ASJC) codes

  • Cell Biology


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