Key result
This review provides an overview of the structure-function of MK5, its role in cardiac structure and function, and the cardiac phenotype of MK5 haplodeficient mice.
MK5 is an emerging regulator of cardiac fibroblast function and cardiac remodeling, though its exact activation pathways remain controversial.
Positions MK5 as a potential therapeutic target for cardiac remodeling; leaves open its exact.
MAP kinase-activated protein kinases (MKs), protein serine/threonine kinases downstream of the MAPKs, regulate a number of biological functions. MK5 was initially identified as a substrate for p38 MAPK but subsequent studies revealed that MK5 activity is regulated by atypical MAPKs ERK3 and ERK4. However, the roles of these MAPKs in activating MK5 remain controversial. The interactome and physiological function of MK5 are just beginning to be understood. Here, we provide an overview of the structure-function of MK5 including recent progress in determining its role in cardiac structure and function. The cardiac phenotype of MK5 haplodeficient mice, and the effect of reduced MK5 expression on cardiac remodeling, is also discussed.
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Sahadevan et al. (2017) conducted a review in Cardiac remodeling. MK5 was evaluated. This review provides an overview of the structure-function of MK5, its role in cardiac structure and function, and the cardiac phenotype of MK5 haplodeficient mice.
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