2023
DOI: 10.1096/fj.202300944rr
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Nintedanib ameliorates osteoarthritis in mice by inhibiting synovial inflammation and fibrosis caused by M1 polarization of synovial macrophages via the MAPK/PI3K‐AKT pathway

Jiangbo Yan,
Gangning Feng,
Yong Yang
et al.

Abstract: Synovial inflammation and fibrosis are important pathological changes associated with osteoarthritis (OA). Herein, we investigated if nintedanib, a drug specific for pulmonary fibrosis, plays a positive role in osteoarthritic synovial inflammation and fibrosis. We assessed the effect of nintedanib on osteoarthritic synovial inflammation and fibrosis in a mouse model of OA created by destabilization of the medial meniscus and a macrophage M1 polarization model created by stimulating RAW264.7 cells with lipopoly… Show more

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Cited by 3 publications
(1 citation statement)
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“…The mechanism involves inhibition of the PI3K-AKT signalling axis [ 15 ]. One study demonstrated that the inhibition of M1 polarization in osteoarthritis synovial macrophages by nintedanib is mediated by the MAPK/PI3K-AKT pathway, resulting in reduced articular cartilage degeneration [ 176 ]. The inhibitory effect of CeO NPs on ROS-induced MAPK production in macrophages may also contribute to the M2 polarization of macrophages.…”
Section: Effects Of Re Nms On Osteogenesis and The Underlying Mechanismsmentioning
confidence: 99%
“…The mechanism involves inhibition of the PI3K-AKT signalling axis [ 15 ]. One study demonstrated that the inhibition of M1 polarization in osteoarthritis synovial macrophages by nintedanib is mediated by the MAPK/PI3K-AKT pathway, resulting in reduced articular cartilage degeneration [ 176 ]. The inhibitory effect of CeO NPs on ROS-induced MAPK production in macrophages may also contribute to the M2 polarization of macrophages.…”
Section: Effects Of Re Nms On Osteogenesis and The Underlying Mechanismsmentioning
confidence: 99%