Marie Besnier, David Coquerel, Julie Favre, Anais Dumesnil, Dominique Guerrot, Isabelle Remy-Jouet, Paul Mulder, Zoubir Djerada, Fabienne Tamion, Vincent Richard, Antoine Ouvrard-Pascaud
Background- We previously showed that Protein Tyrosine Phosphatase 1B inactivation (PTP1B-/- ) in mice improved left ventricular (LV) angiogenesis, perfusion, remodeling and function, and limits endothelial dysfunction after myocardial infarction. However, whether PTP1B inactivation slows aging-associated cardiovascular dysfunction remains unknown. Methods and Results- WT and PTP1B-/- mice were allowed to age until 18 months. Compared to old WT in which aging increased the LV mRNA expression of PTP1B, old PTP1B-/- mice had: 1) reduced cardiac hypertrophy with decreased LV mRNA levels of hypertrophic markers, atrial and brain natriuretic peptides; 2) lower LV fibrosis (collagen: WT 16{plus minus}3, PTP1B-/- 5{plus minus}3 %, p<0...
March 23, 2018: American Journal of Physiology. Heart and Circulatory Physiology