Abstract
Mitogen-activated protein (MAP) kinases comprise a well-studied family of serine/threonine protein kinases involved in signal transduction pathways that control multiple cellular processes. The extracellular signal-regulated kinase (ERK1/2) cascade is a central MAP kinase pathway that transmits signals from the cell surface to substrates either in the nucleus or in the cytoplasm. The transmission of the signal through the ERK1/2 cascade is mediated by phosphorylation and activation of protein kinases. Abnormal regulation of the ERK1/2 signals has been linked to diseases and recent work clearly implicated ERK1/2 signaling in the development of cardiac pathologies. Understanding the underlying mechanism and the consequences of the aberrant modulation of ERK1/2 cascade will lead to the development of pharmacologic inhibitors for the treatment of these cardiac disorders.
Highlights
A proportion of inherited cardiomyopathies display deregulated Mitogen-activated protein (MAP) kinase signaling
A proportion of inherited cardiomyopathies display deregulated MAP kinase signaling. As these diseases are a major cause of cardiac disease in human, it is not surprising that the MAP kinase signaling continues to be the subject of intense researches for future pharmacological intervention
We recently demonstrated an aberrant increase in ERK1/2 activity in hearts from a mouse model of the disease [42]
Summary
A proportion of inherited cardiomyopathies display deregulated MAP kinase signaling. As these diseases are a major cause of cardiac disease in human, it is not surprising that the MAP kinase signaling continues to be the subject of intense researches for future pharmacological intervention. The development of molecules targeting this pathway has focused mostly on the development of small-molecule inhibitors. This review will gather information on MAP kinase signaling, focusing on the ERK1/2 branch and will discuss important research progresses in the field of inherited cardiomyopathies. The recent years provided some clues to explain the pathogenesis of such disease, involving ERK1/2, which might open novel and promising perspectives for future clinical trials
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