Fibroblast Smad7 Induction Protects the Remodeling Pressure-Overloaded Heart.

ABSTRACT:

Background

Cardiac fibroblast activation contributes to adverse remodeling, fibrosis, and dysfunction in the pressure-overloaded heart. Although early fibroblast TGF-β (transforming growth factor-β)/Smad (small mother against decapentaplegic)-3 activation protects the pressure-overloaded heart by preserving the matrix, sustained TGF-β activation is deleterious, accentuating fibrosis and dysfunction. Thus, endogenous mechanisms that negatively regulate the TGF-β response in fibroblasts may be required to protect from progressive fibrosis and adverse remodeling. We hypothesized that Smad7, an inhibitory Smad that restrains TGF-β signaling, may be induced in the pressure-overloaded myocardium and may regulate fibrosis, remodeling, and dysfunction.

Methods

The effects of myofibr

SUBMITTER: Humeres C 

PROVIDER: S-EPMC11257802 | biostudies-literature | 2024 Jul

REPOSITORIES: biostudies-literature