GIT2 negatively regulates the NF-κB pathway directly or indirectly by regulating TRAF3 expression to promote osteogenic differentiation of BMSCs.

Yanna Wang, Changyuan Wang, Ying Gong, Qingchen Li, Mozhen Liu, Huijun Sun

Department of Clinical Pharmacology, College of Pharmacy, Dalian Medical University, 9 West Section, Lvshun South Road, Dalian, Lvshunkou District 116044, China.Department of Clinical Pharmacology, College of Pharmacy, Dalian Medical University, 9 West Section, Lvshun South Road, Dalian, Lvshunkou District 116044, China. · pubmed

Paper

Abstract

Osteoporosis (OP) is a common disease of aging, which is closely related to the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). DNA damage, as a senescence-associated secretory phenotype (SASP), plays an important role in aging diseases including OP. GIT2 has been identified as a DNA repair gene and alleviates aging-related phenotypes. However, the relationship between GIT2 and osteogenic differentiation of BMSCs remains unclear.

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Research summary

GIT2 regulates TRAF3 expression to promote osteogenic differentiation of BMSCs, which may have implications for osteoporosis treatment. The paper addresses a mechanism related to aging and bone health, linking GIT2 to osteogenic differentiation, which is relevant to understanding age-related diseases.

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