:
Pathological bone loss diseases (osteolysis, Paget’s diseases) are commonly caused by the over differentiation
and activity of osteoclasts. The Rho GTPases family members Rac1/2 (Rac1 and Rac2) have been reported for their special
role in exerting multiple cellular functions during osteoclastic differentiation, which including the most prominent function
on dynamic actin cytoskeleton rearranging. Besides that, the increasing studies demonstrated the regulating effects of
Rac1/2 on osteoclastic cytoskeletal organization is through the GEFs member Dock5. Although the amount of relevant studies on this topic still limited, there are several excellent studies have been reported for extensively explored the molecular
mechanisms involved in Rac1/2 and Dock5 during the osteoclastogenesis regulation, as well as their role as the therapeutic
target in bone loss disesases. Herein in this review, we aim to focus on recent advances studies for extensively understanding the role of Rho GTPases Rac1/2 and Dock5 in osteoclastogenesis, as well as their role as a potential therapeutic target in
regulating osteoclastogenesis.
