Loss of talin in cardiac fibroblasts results in augmented ventricular cardiomyocyte hypertrophy in response to pressure overload
Natalie A. Noll, Lance A. Riley, Christy Moore, Lin Zhong, Mathew R. Bersi, James West, Roy Zent, W. David Merryman
Abstract
The role of talins has been previously studied in cardiomyocytes; however, these mechanotransductive proteins that are members of the focal adhesion complex have not been examined in cardiac fibroblasts previously. We hypothesized that loss of talins in cardiac fibroblasts would reduce interstitial fibrosis in the heart with a pressure overload model. However, we found that although loss of talins did not alter fibrosis, it did result in cardiomyocyte and ventricular hypertrophy.
Topics & Concepts
Pressure overloadFibrosisMuscle hypertrophyInternal medicineCardiologyCardiac fibrosisCardiac hypertrophyMedicineMyofibroblastCellular Mechanics and InteractionsCardiomyopathy and Myosin StudiesCardiovascular Effects of Exercise