Results 91 to 100 of about 28,700 (204)
ROS‐Targeted Nanomotor Therapy in OA: Cartilage Protection and Pain Relief
ROS‐responsive NM@MET nanomotors utilize elevated ROS in osteoarthritic joints to promote deep penetration into cartilage and synovium and enable sustained metformin release. By scavenging ROS, regulating NRF2/KEAP1 signaling, protecting chondrocytes, suppressing synovial inflammation, and attenuating nociceptive signaling, NM@MET alleviates pain and ...
Meng Zheng +19 more
wiley +1 more source
THBS1+ Macrophages Exacerbate Modic Changes via SDC4‐Dependent Activation of NLRP3 Inflammasome
The illustration of THBS1+ macrophages exacerbate MCs via SDC4‐dependent activation of the NLRP3 inflammasome. THBS1+ macrophage subpopulation was identified in MCs through single‐cell RNA sequencing. C. acnes and its metabolites activate THBS1 expression in macrophages via the TLR signaling pathway.
Xiangxi Kong +16 more
wiley +1 more source
S100A8/A9‐high macrophages are markedly enriched in the stenotic intestinal tissue of patients with Crohn's disease. These profibrotic macrophages secrete mCCL6 in a STAT3‐dependent manner. mCCL6 and its human ortholog hCCL15 activate fibroblasts via the CCR1 receptor, thereby driving excessive collagen deposition.
Shu Wang +12 more
wiley +1 more source
ABSTRACT Osteoarthritis (OA) is a progressive and disabling joint disease driven by oxidative stress, chondrocyte senescence and extracellular matrix (ECM) degradation, yet lacks effective disease‐modifying treatments. In this study, we identified miR‐197‐3p as a previously unrecognized, cartilage‐protective miRNA significantly downregulated in both ...
Xuejie Cai +11 more
wiley +1 more source
Knee osteoarthritis (OA) causes pain and disability, and autologous adipose-derived stem cell (ASC) therapy has emerged as a regenerative treatment option.
Naoki Nakano +10 more
doaj +1 more source
NSUN2‐mediated m5C modification cooperates with ALYREF to stabilize and export IP3R3 mRNA, increasing IP3R3 expression and Ca2 + overload in chondrocytes. This signaling promotes mitochondrial dysfunction, NLRP3 inflammasome activation, and senescence, thereby accelerating osteoarthritis progression.
Guping Mao +8 more
wiley +1 more source
Cartilage injury promotes local fibrinogen deposition, which accelerates monosodium urate crystallization and activates integrin‐mediated matrix‐degradation. This self‐amplifying cycle drives gout‐related cartilage erosion. Disrupting fibrinogen deposition or restoring the cartilage barrier could interrupt this vicious cycle.
Hanlin Xu +7 more
wiley +1 more source

