Deletion of Interleukin-6 Attenuates Pressure Overload-Induced Left Ventricular Hypertrophy and Dysfunction.

ABSTRACT:

Rationale

The role of interleukin (IL)-6 in the pathogenesis of cardiac myocyte hypertrophy remains controversial.

Objective

To conclusively determine whether IL-6 signaling is essential for the development of pressure overload-induced left ventricular (LV) hypertrophy and to elucidate the underlying molecular pathways.

Methods and results

Wild-type and IL-6 knockout (IL-6(-/-)) mice underwent sham surgery or transverse aortic constriction (TAC) to induce pressure overload. Serial echocardiograms and terminal hemodynamic studies revealed attenuated LV hypertrophy and superior preservation of LV function in IL-6(-/-) mice after TAC. The extents of LV remodeling, fibrosis, and apoptosis were reduced in IL-6(-/-) hearts after TAC. Transcriptional and protein assays of my

SUBMITTER: Zhao L 

PROVIDER: S-EPMC4902783 | biostudies-literature | 2016 Jun

REPOSITORIES: biostudies-literature