Hyperphosphorylation of mouse cardiac titin contributes to transverse aortic constriction-induced diastolic dysfunction.

ABSTRACT:

Rationale

Mechanisms underlying diastolic dysfunction need to be better understood.

Objective

To study the role of titin in diastolic dysfunction using a mouse model of experimental heart failure induced by transverse aortic constriction.

Methods and results

Eight weeks after transverse aortic constriction surgery, mice were divided into heart failure (HF) and congestive heart failure (CHF) groups. Mechanical studies on skinned left ventricle myocardium measured total and titin-based and extracellular matrix-based passive stiffness. Total passive stiffness was increased in both HF and CHF mice, and this was attributable to increases in both extracellular matrix-based and titin-based passive stiffness, with titin being dominant. Protein expression and titin exon microa

SUBMITTER: Hudson B 

PROVIDER: S-EPMC3191198 | biostudies-literature | 2011 Sep

REPOSITORIES: biostudies-literature