Evidence for calreticulin attenuation of cardiac hypertrophy induced by pressure overload and soluble agonists.

ABSTRACT: While calreticulin has been shown to be critical for cardiac development, its role in cardiac pathology is unclear. Previous studies have shown the detrimental effects on the heart of sustained germline calreticulin overexpression, yet without calreticulin, the heart does not develop normally. Thus, carefully balanced calreticulin levels are required for the heart to develop and to function properly into adulthood. But what happens to calreticulin levels, and how is this regulated, during cardiac hypertrophy, during which the fetal gene program is reactivated, at least partially? Our working hypothesis was that c-Src, a kinase whose activity we previously found to be correlated with calreticulin expression, was involved with calreticulin in regulating the response to hypertrophic signals.

SUBMITTER: Papp S 

PROVIDER: S-EPMC2832134 | biostudies-literature | 2010 Mar

REPOSITORIES: biostudies-literature