ArticleAmerican journal of translational research2021
Silencing of TLR7 protects against lipopolysaccharide-induced chondrocyte apoptosis and injury by blocking the p21-mediated JAK2/STAT3 pathway.
Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Exosomes derived from hypoxia-preconditioned M2 macrophages alleviate degeneration in knee osteoarthritis through the miR‑124‑3p/STAT3 axis.Journal of translational medicine · 2025Article
- Osteoclast Activation and Inflammatory Bone Diseases: Focusing on Receptors in Osteoclasts.Journal of inflammation research · 2025Review
- Key Role of STAT3 in Osteoarthritis: From Pathogenic Mechanisms to Targeted Therapy.International journal of nanomedicine · 2025Review
- Identification and validation of FPR1, FPR2, IL17RA and TLR7 as immunogenic cell death related genes in osteoarthritis.Scientific reports · 2023Article
- Consensus cluster analysis of apoptosis-related genes in patients with osteoarthritis and their correlation with immune cell infiltration.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Involvement of toll-like receptor 7 (TLR7) in the immune response has been reported in diverse inflammatory diseases. However, the role of TLR7 in the pathogenesis of osteoarthritis (OA) is poorly understood. In this study, we sought to investigate the contribution of TLR7 in regulating chondrocyte apoptosis, inflammation, and degradation of the extracellula matrix (ECM), and its underlying mechanisms. We found that TLR7 expression was increased in cartilage tissues of OA patients and in lipopolysaccharide (LPS)-induced chondrocytes. Silencing of TLR7 alleviated LPS-induced chondrocyte apoptosis, inflammation, and ECM degradation. Mechanistically, TLR7 silencing inhibited the JAK2/STAT3 signaling pathway by inducing p21 expression. Moreover, p21 knockdown and colivein (an activator of JAK2/STAT3 signaling) partially rescued the suppressive role of TLR7 silencing on chondrocyte apoptosis, the inflammatory response, and ECM underproduction. Taken together, our data revealed that knockdown of TLR7 attenuated chondrocyte apoptosis and injury by blocking the p21-mediated JAK2/STAT3 pathway, suggesting that TLR7 may be a therapeutic target in OA.
Indexed as
Identifiers
35035696PMC8748165W4206886353What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.