MKP-1 Modulates Mitochondrial Transcription Factors, Oxidative Phosphorylation, and Glycolysis.

ABSTRACT: Sepsis is the leading cause of death in the world. Recent reports suggest that in response to sepsis, metabolism of macrophages switches from oxidative phosphorylation to aerobic glycolysis. MAPK phosphatase (MKP)-1 (also known as DUSP1) localized in the nucleus and preferentially dephosphorylates p38 and JNK. MKP-1 controls the expression of numerous inflammatory genes and transcription factors, thereby regulating innate and adaptive immunity. MKP-1-deficient animals exhibit aberrant metabolic responses following bacterial infections with a markedly increased mortality in response to sepsis. Because metabolic reprogramming modulates immune responses to TLR-4 activation, we investigated the effect of MKP-1 deficiency on mitochondrial electron transport chains involved in oxidative phosphor

SUBMITTER: Bauerfeld C 

PROVIDER: S-EPMC7646982 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature