Genetic ablation of fibroblast activation protein alpha attenuates left ventricular dilation after myocardial infarction.

ABSTRACT:

Introduction

Regulating excessive activation of fibroblasts may be a promising target to optimize extracellular matrix deposition and myocardial stiffness. Fibroblast activation protein alpha (FAP) is upregulated in activated fibroblasts after myocardial infarction (MI), and alters fibroblast migration in vitro. We hypothesized that FAP depletion may have a protective effect on left ventricular (LV) remodeling after MI.

Materials and methods

We used the model of chronic MI in homozygous FAP deficient mice (FAP-KO, n = 51) and wild type mice (WT, n = 55) to analyze wound healing by monocyte and myofibroblast infiltration. Heart function and remodeling was studied by echocardiography, morphometric analyses including capillary density and myocyte size, collagen content and in v

SUBMITTER: Hoffmann DB 

PROVIDER: S-EPMC7935287 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature