Table 2 Role of various cells in the pathogenesis of OA
Cell types | Molecules or signals involved during OA | Effect | Refs |
|---|---|---|---|
Chondrocytes | p16-pRb pathway | p16 induces senescence in OA chondrocytes via the p16-pRb pathway | [84] |
SASP (IL-1β, IL-6, TNF-α) | Senescent chondrocytes release SASP to destabilize the ECM, thereby initiating OA progression | ||
CCN1 | CCN1 signaling aggravates cartilage inflammation and matrix degradation. | [90] | |
Amyloid protein | The amyloid protein promotes abnormal gene expression, mitochondrial dysfunction, and cell death in OA chondrocytes | [85] | |
Osteoblast | TGF β1; TGF β/ Smad pathway | Induce subchondral angiogenesis to indirectly affect chondrocyte | |
RANKL | Stimulate osteoclast differentiation and enhance bone resorption | ||
VEGF | Stimulate angiogenesis to indirectly affect chondrocyte | ||
SOST | The lack of SOST aggravate OA by producing different degrees of apoptosis in the body to affect subchondral bone homeostasis | ||
Osteoclast | Calcium-phosphate complex | Promotes the secretion of MMP-3, MMP-13 by chondrocytes, leading to cartilage degeneration | [102] |
TGF β/Smad pathway | Promote the hypertrophic differentiation of chondrocyte | ||
Osteocyte | RANKL/OPG; RANK-RANKL-OPG system | Induce osteoclast differentiation and enhance bone resorption | |
VEGF; mTORC1 pathway | Indirect regulation of chondrocytes by stimulating angiogenesis | [93] | |
Synovium fibroblasts | AMPK and p38 pathways; APLN; PI3K and ERK pathway | Knockdown of APLN expression could ameliorated changes in OA cartilage severity | [103] |
Musculoskeletal cells | Sarcolipin | Sarcolipin secreted by senescent muscle cells promote skeletal muscle fibrosis and ultimately lead to sarcopenia, thereby accelerating the development of OA in terms of biomechanical mechanisms | [104] |
Myokine, myostatin; Wnt/β-catenin signaling | The muscle released myokine, myostatin inhibits osteogenic differentiation by suppressing Wnt/β-catenin signaling | [105] |