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LncPVT1 promotes cartilage degradation in diabetic OA mice by downregulating miR-146a and activating TGF- β/SMAD4 signaling
ConclusionsOur results demonstrate LncRNA PVT1 is involved in cartilage degradation in diabetic OA and correlated with disease severity. Efficiency of ad-siRNA-PVT1 in controlling joint inflammation in diabetic OA mice is associated with the suppression of the expression of miR-146a, pro-inflammatory cytokines and activation of TGF- β/SMAD4 pathway.
Source: Journal of Bone and Mineral Metabolism - February 10, 2021 Category: Orthopaedics Source Type: research

Hypoxia-Induced Fibroblast Growth Factor 11 Stimulates Osteoclast-Mediated Resorption of Bone
This study suggests FGF11 as a novel factor driving pathological bone resorption in osteolytic disease and as a potential target for the development of new anti-resorptive therapeutic agents.
Source: Calcified Tissue International - January 17, 2017 Category: Orthopaedics Source Type: research

MicroRNA-20a negatively regulates expression of NLRP3-inflammasome by targeting TXNIP in adjuvant-induced arthritis fibroblast-like synoviocytes
Conclusion Taken together, these results indicate that miR-20a may play a pivotal role in the NLRP3-inflammasome by targeted inhibit TXNIP expression in AA FLSs.
Source: Joint Bone Spine - February 29, 2016 Category: Orthopaedics Source Type: research

Increased RANKL-mediated osteoclastogenesis by interleukin-1β and endoplasmic reticulum stress
Conclusions Osteoclastogenesis by IL-1β and/or ER stress is mainly associated with upregulation of eIF2α, GRP78, PERK and IRE1. These results suggest that the signaling pathway of ER stress-induced osteoclast formation might be a new therapeutic target to prevent inflammatory and destructive arthritic disease such as RA and diverse osteoporosis.
Source: Joint Bone Spine - December 12, 2014 Category: Orthopaedics Source Type: research

Connexin43 enhances the expression of osteoarthritis-associated genes in synovial fibroblasts in culture
Conclusions: Increasing or decreasing Cx43 expression alone was sufficient to alter the levels of catabolic and inflammatory genes expressed by synovial cells. The NFkappaB cascade mediated the effect of Cx43 on the expression of a subset of these OA-associated genes. As such, Cx43 may be involved in joint pathology during OA, and targeting Cx43 expression or function may be a viable therapeutic strategy to attenuate the catabolic and inflammatory environment of the joint during OA.
Source: BMC Musculoskeletal Disorders - December 11, 2014 Category: Orthopaedics Authors: Aditi GuptaCorinne NigerAtum BuoEric EidelmanRichard ChenJoseph Stains Source Type: research