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Chuangxin Lin

Researcher at Southern Medical University

Publications -  11
Citations -  470

Chuangxin Lin is an academic researcher from Southern Medical University. The author has contributed to research in topics: Osteoarthritis & Synovitis. The author has an hindex of 6, co-authored 8 publications receiving 215 citations.

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Synovial macrophage M1 polarisation exacerbates experimental osteoarthritis partially through R-spondin-2.

TL;DR: 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.
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Blocking PI3K/AKT signaling inhibits bone sclerosis in subchondral bone and attenuates post-traumatic osteoarthritis.

TL;DR: 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.
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Activation of mTORC1 in subchondral bone preosteoblasts promotes osteoarthritis by stimulating bone sclerosis and secretion of CXCL12.

TL;DR: 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.
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Hesperidin inhibits synovial cell inflammation and macrophage polarization through suppression of the PI3K/AKT pathway in complete Freund's adjuvant-induced arthritis in mice.

TL;DR: It is concluded that HSN has significant anti-inflammatory activities and reduces the potential of MMPs in rheumatoid arthritis and the degree of polarization of macrophages to M1.
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Mechanical stress contributes to osteoarthritis development through the activation of transforming growth factor beta 1 (TGF-β1).

TL;DR: Mechanical stress contributes to osteoarthritis development through the activation of transforming growth factor beta 1 (TGF-β1), which is responsible for chondrocyte apoptosis and cartilage degeneration in OA.