Loss of β-catenin in resident cardiac fibroblasts attenuates fibrosis induced by pressure overload in mice.

ABSTRACT: Cardiac fibrosis is characterized by excessive extracellular matrix deposition that contributes to compromised cardiac function and potentially heart failure. Cardiac pressure overload resulting from trans-aortic constriction in mice leads to cardiac fibrosis and increased Wnt/β-catenin signaling in cardiac fibroblasts. Here, we conditionally induce β-catenin loss of function in resident cardiac fibroblasts using Tcf21 ^MerCreMer or in activated cardiac fibroblasts using periostin (Postn) ^MerCreMer . We show that β-catenin loss of function in cardiac fibroblasts after trans-aortic constriction significantly preserves cardiac function, and reduces interstitial fibrosis but does not alter the numbers of activated or differentiated cardiac fibroblasts in vivo. However, β-

SUBMITTER: Xiang FL 

PROVIDER: S-EPMC5620049 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature