Regulating osteogenic differentiation of bone marrow mesenchymal stem cells by mTORC1 signaling pathway inhibits bone defect repair in mice.

ABSTRACT:

Background

Bone defects caused by traumatic injuries and orthopedic diseases have emerged as the most common challenges in contemporary orthopedics, characterized by treatment difficulty, long treatment time, and high economic costs. This study aims to demonstrate that the activated mTOR pathway in mesenchymal stromal cells regulates the bone repair process.

Methods

Initially, the mammalian target of rapamycin (mTOR) pathway-activated mouse model was constructed by specifically knocking down the tuberous sclerosis complex 1 (TSC1) molecule in bone marrow mesenchymal stem cells (BMMSCs). Then, the differences in bone repair between transgenic mice and littermate control mice in a single-layer cortical bone defect model were evaluated by histological, immunohistochemical, and

SUBMITTER: Huang Z 

PROVIDER: S-EPMC12482767 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature