Mitogen-activated protein kinase (MAPK)-activated protein kinase (MK2) is
exclusively regulated by p38 MAPK in vivo. Upon activation of p38 MAPK, MK2
binds with p38 MAPK, leading to phosphorylation of TTP, Hsp27, Akt, and Cdc25 that
are involved in regulation of various essential cellular functions. In this review, we discuss current knowledge about molecular
mechanisms of MK2 in regulation of TNF-α production, NADPH oxidase activation, neutrophil migration, and
DNA-damage-induced cell cycle arrest which are involved in the molecular pathogenesis of acute lung injury, pulmonary
fibrosis, and non-small-cell lung cancer. Collectively current and emerging new information indicate that developing
MK2 inhibitors and blocking MK2-mediated signal pathways are potential therapeutic strategies for treatment of inflammatory
and fibrotic lung diseases and lung cancer.
Keywords: Acute lung injury, inflammation, lung cancer, MK2, MAPK, pulmonary fibrosis.
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