Sex-specific phenotypes in the aging mouse heart and consequences for chronic fibrosis
Aude Angelini, Jesús Ortiz-Urbina, JoAnn Trial, Anilkumar K. Reddy, Anna Malovannaya, Antrix Jain, Mark L. Entman, George E. Taffet, Katarzyna A. Cieslik
Abstract
The aging heart develops diastolic dysfunction because of increased collagen deposition. We attempted to reduce collagen expression in the old heart by activating AMPK using AICAR. An improvement of diastolic function and reduction of cardiac fibrosis was found only in the female heart and correlated with decreased procollagen expression and increased degradation of the transcription factor Gli1. Male hearts display blunted AICAR-dependent AMPK activation and therefore this treatment had no benefits for the male mice.
Topics & Concepts
Internal medicineEndocrinologyVentricleFibrosisDiastoleAMPKMedicineVentricular remodelingExtracellular matrixMyocardial infarctionBiologyPhosphorylationProtein kinase ACell biologyBlood pressureCardiac Fibrosis and RemodelingCardiovascular Function and Risk FactorsTissue Engineering and Regenerative Medicine