Platelet-rich plasma pretreatment protects anterior cruciate ligament fibroblasts correlated with PI3K-Akt-mTOR pathway under hypoxia condition

Exosomes derived from tendon stem/progenitor cells enhance tendon-bone interface healing after rotator cuff repair in a rat model

“…The AKT/mTOR signaling pathway participates in cellular proliferation, differentiation, apoptosis, and metastasis, giving it a crucial role in various diseases [ [52] , [53] , [54] ]. Reports suggest that the AKT/mTOR signaling pathway may serve as a crucial node in tendon differentiation [ 55 ]. A recent study observed downregulation of the AKT/mTOR signaling pathway in a rat rotator cuff injury model, resulting in decreased protein synthesis and subsequent muscle atrophy [ 56 ].…”

3D-printed hydrogel particles containing PRP laden with TDSCs promote tendon repair in a rat model of tendinopathy

“…In other studies, inhibition of the PI3K-AKT pathway reduced the inflammatory response [ 53 ]. Cao et al suggested that PRP pretreatment of tendon cells could downregulate PI3K-AKT-mTOR pathway to protect tendon cells from injury caused by hypoxia [ 54 ]. Xue et al found that the inflammatory response during arthritis could be reduced by downregulating the PI3K-AKT-mTOR pathway.…”

Melatonin alleviates oxidative stress-induced injury to nucleus pulposus-derived mesenchymal stem cells through activating PI3K/Akt pathway

“…It was reported by Li that Cerebrospinal fluid-derived extracellular vesicles could enhance vascular regeneration by activating the PI3K/AKT pathway, hence improving motor function recovery after spinal cord injury [ 47 ].More importantly, many studies have shown that PI3K/Akt is closely related to apoptosis or senescence changes in MSCs and NP cells [ 48 , 43 ]. For example, Cao et al [ 49 ] found that Platelet-rich plasma pretreatment can protect anterior cruciate ligament fibroblasts by increasing cell viability, proliferation and migration and reducing apoptosis. It means that the activation of PI3K/Akt could maintain the balance between synthesis and metabolism of cells to avoid degeneration.…”