• Publications
  • Influence
Synovial macrophage M1 polarisation exacerbates experimental osteoarthritis partially through R-spondin-2
TLDR
The results show that promoting the macrophage M1 polarisation leads to exacerbation of experimental OA partially through secretion of Rspo2 and activation of β-catenin signalling in chondrocytes.
mTORC1 regulates PTHrP to coordinate chondrocyte growth, proliferation and differentiation
TLDR
It is demonstrated that dynamically controlled mTORC1 activity is crucial to coordinate chondrocyte proliferation and differentiation partially through regulating Gli2/PTHrP during endochondral bone development.
Macrophages regulate the progression of osteoarthritis.
Metformin attenuates cartilage degeneration in an experimental osteoarthritis model by regulating AMPK/mTOR
TLDR
Metformin effectively alleviated cartilage degradation and aging through regulation of the AMPK/mTOR signaling pathways, suggesting that it could be an effective treatment for OA.
MFG-E8 regulated by miR-99b-5p protects against osteoarthritis by targeting chondrocyte senescence and macrophage reprogramming via the NF-κB pathway
TLDR
It is found that MFG-E8 expression was downregulated both locally and systemically as OA advanced in patients with OA and in mice after destabilization of the medial meniscus surgery (DMM) to induce OA, and intra-articular injection of MFG -E8 is identified as a potential therapeutic target for OA prevention and treatment.
Blocking PI3K/AKT signaling inhibits bone sclerosis in subchondral bone and attenuates post‐traumatic osteoarthritis
TLDR
I inhibition of PI3K/AKT/NF‐κB axis was able to prevent aberrant bone formation and attenuate cartilage degeneration in OA mice and was found to enhance preosteoblast proliferation, differentiation, and expression of MMP‐13 by activating NF‐κBs pathway.
Positive‐Feedback Regulation of Subchondral H‐Type Vessel Formation by Chondrocyte Promotes Osteoarthritis Development in Mice
TLDR
A positive‐feedback regulation of H‐type vessel formation in subchondral bone by articular chondrocyte nutrient‐sensing mTORC1 signaling is essential for the pathogenesis and progression of OA.
Activation of mTORC1 in subchondral bone preosteoblasts promotes osteoarthritis by stimulating bone sclerosis and secretion of CXCL12
TLDR
It is demonstrated that mTORC1 activation in subchondral preosteoblasts is not sufficient to induce OA, but can induce aberrant sub chondral bone formation and secrete of Cxcl12 to accelerate disease progression following surgical destabilization of the joint.
...
...