Fracture healing is a poorly understood process, wherein osteoblast migration and proliferation are the fundamental bone healing processes, and GIT1 gene is a key regulator of bone mass and osteoblast cell migration [
17,
18] Furthermore, GIT1 is the key to fracture healing, and a lot of key amino acids could influence fracture healing after GIT1 gene deletion [
19,
20]. Therefore, our study aims to explore the underlying mechanism of GIT1 and tibial plateau facture and chondrocyte cells.
Our study found that GIT1 gene deletion could block the healing of tibial plateau fractures, wherein chondrocytes exist persistently and delay cell differentiation. Fracture healing is a process of post natal repair, and many molecular mechanisms could control cell differentiation and embryo development [
21]. Consistently, chondrocytes play an essential role in the process of repairing osteoarthritis [
22]. It is well-known fact that vascular endothelial growth factor (VEGF) plays a crucial role during endochondral bone formation in hypertrophic cartilage remodeling, ossification, and angiogenesis [
23]. In addition, a previous study showed that the increase of bone mass of GIT1 wild type control GIT1 knockout (KO) mice is 2.3 times that of wild type GIT1 knockout (KO) mice control, causing bone defects, and expression of GIT1 could be found in osteoclast and chondrocyte cells [
18]. Similarly, a variety of growth factors have been used in order to accelerate the healing process including platelet-derived growth factor (PDGF) and TGF-β, and PDGF could regulate chondrocyte proliferation through the activation of GIT1, which proves that GIT1 gene deletion could delay the healing process [
24,
25]. Moreover, a previous study indicated that differentiation and maturation of chondrocytes are crucial in fracture healing, involved in the entire process of fracture healing, which is consistent with our study results [
26]. Likewise, GIT1 deficiency impairs osteoclast functioning, and is required for osteoclasts differentiation, which could prove our results [
18]. Additionally, GIT1 is capable of regulating fracture healing through the TGF-β signaling pathway, and previous studies confirmed that TGF-β could inhibit cell growth by controlling chondrocyte synthesis and promoting the differentiation process of the chondrocytes [
20,
27], so GIT1 gene deletion is capable of delaying chondrocyte differentiation. Besides, GIT1 gene deletion could regulate the fracture healing process, and findings suggest that chondrocytes differentiation is affected by the loss of GIT1 [
28].
Additionally, GIT1 gene deletion could contribute to the decreasing chondrocyte proliferation and apoptosis after tibial plateau fracture. Furthermore, a major function of GIT1 is to regulate cytoskeletal dynamics to facilitate cell spreading and spatial targeting, and GIT1 is a potential target for the treatment of osteoporosis [
17,
18]. In addition, a number of growth factors such as PDGF could promote the proliferation of chondrocytes effectively, indicating that GIT1 gene deletion could inhibit cell proliferation [
24]. Similarly, a study found that GIT1 is involved in the normal progression of bone injury after repair, and GIT1 gene KO mice could also decrease chondrocytes proliferation and inhibit apoptosis, which is consistent with our results [
28]. Moreover, integrin-β1 and GIT1 gene are positively correlated, and integrin-β1 has the ability to regulate chondrocyte proliferation and apoptosis, demonstrating that GIT1 gene deletion could significantly decrease chondrocyte apoptosis [
22].