Metabolic dysfunction consistent with premature aging results from deletion of Pim kinases.

ABSTRACT:

Rationale

The senescent cardiac phenotype is accompanied by changes in mitochondrial function and biogenesis causing impairment in energy provision. The relationship between myocardial senescence and Pim kinases deserves attention because Pim-1 kinase is cardioprotective, in part, by preservation of mitochondrial integrity. Study of the pathological effects resulting from genetic deletion of all Pim kinase family members could provide important insight about cardiac mitochondrial biology and the aging phenotype.

Objective

To demonstrate that myocardial senescence is promoted by loss of Pim leading to premature aging and aberrant mitochondrial function.

Methods and results

Cardiac myocyte senescence was evident at 3 months in Pim triple knockout mice, where all 3 isofo

SUBMITTER: Din S 

PROVIDER: S-EPMC4254755 | biostudies-literature | 2014 Jul

REPOSITORIES: biostudies-literature