Deletion of fibro-adipogenic progenitors-specific follistatin impairs muscle function and accelerates skeletal muscle atrophy in obese mice.

ABSTRACT:

Background

Follistatin is a potent regulator of various TGF-β superfamily members, including myostatin (MSTN) and activin A. Previous studies have shown that follistatin is crucial in enhancing myogenesis during acute muscle injury. The mechanism by which fibro-adipogenic progenitors (FAPs)-specific follistatin influences muscle homeostasis in obese mice remains unknown. Therefore, we investigated the physiological role of follistatin in PDGFRα-positive FAPs in the regulation of muscle homeostasis and exercise in obese mice.

Methods

A PDGFRα-specific follistatin knockout (follistatin KO) mouse model was generated using PDGFRα-GFP-CreER^T2 (PDGFRα-GCE) and follistatin^flox/flox mice. These mice were fed a 60% high-fat diet (HFD) for 20 weeks, followed by a

SUBMITTER: Aslam MR 

PROVIDER: S-EPMC12752164 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature