ReviewBone research2024
Cross-talk of inflammation and cellular senescence: a new insight into the occurrence and progression of osteoarthritis.
Review in Bone research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
119 citing papers in PubMed.
- Comparative efficacy of ultrasound-guided intra-articular injection of platelet-rich plasma (PRP), hydrolyzed type I collagen, and hyaluronic acid in patients with knee osteoarthritis: a randomized controlled trial.Future science OA · 2026Article
- Stem cell senescence as a regenerative bottleneck in age-related skeletal degeneration: Mechanistic crosstalk and translational strategies.Regenerative therapy · 2026Review
- Nanoimmunomodulation for cartilage repair in osteoarthritis: reprogramming the inflammatory joint microenvironment.International journal of pharmaceutics: X · 2026Review
- A biomimetic chondrocyte membrane-camouflaged tFNA nanoplatform for reprogramming the cartilage-synovium axis in osteoarthritis.Materials today. Bio · 2026Article
- Evaluation of Spontaneous Pain in a Monosodium Iodoacetate-Induced Mouse Model of Osteoarthritis Using the Mouse Grimace Scale.Biomedicines · 2026Article
- Endocrine‑metabolic imbalance drives osteoarthritis: From whole‑joint pathobiology to precision therapy (Review).International journal of molecular medicine · 2026Review
- Association between Modified Cardiometabolic Index and rheumatoid arthritis: the mediating role of phenotypic age acceleration.Clinical rheumatology · 2026Article
- Bioinformatic identification of THY1 as a target in osteoarthritis and its effects on chondrocyte senescence and apoptosis.Functional & integrative genomics · 2026Article
- Piezo1 accelerates osteoarthritis progression via promotion of HBB-dependent oxidative phosphorylation.The Journal of biological chemistry · 2026Article
- Injectable polysaccharide hydrogel microspheres integrated with BPNS-ZnO nanocomposites restore redox homeostasis and protect cartilage in osteoarthritis.Materials today. Bio · 2026Article
- Cross-Tissue Transcriptomic Convergence Identifies a Leuko-Cyte-Shared, Myeloid-Enriched Inflammatory Program in Frailty and Osteoarthritis.International journal of molecular sciences · 2026Article
- Article
- Advances in heterogeneity and classification of osteoarthritis.Bone research · 2026Review
- [Osteoarthritis: epidemiology, pathophysiology, and conservative treatment options].Innere Medizin (Heidelberg, Germany) · 2026Review
- Cryogel-based therapeutic platforms for disease modification in osteoarthritis.npj biomedical innovations · 2026Review
- A microprotein encoded by FERMT3 modulates endothelial cell protein catabolism and induces cell cycle arrest and senescence.Cell communication and signaling : CCS · 2026Article
- Effects of the space environment on articular cartilage homeostasis: a review.NPJ microgravity · 2026Review
- Multi-omics analysis positions DNA2 at the interface of genome integrity programs and tumor behavior in pan-cancer.Functional & integrative genomics · 2026Article
- Cellular senescence as a therapeutic target for aging intervention.Biomedical journal · 2026Review
- Deletion of TOP2B promoter using CRISPR-Cas9 induces senescence in HEK 293T cells.Biochemistry and biophysics reports · 2026Article
59 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) poses a significant challenge in orthopedics. Inflammatory pathways are regarded as central mechanisms in the onset and progression of OA. Growing evidence suggests that senescence acts as a mediator in inflammation-induced OA. Given the lack of effective treatments for OA, there is an urgent need for a clearer understanding of its pathogenesis. In this review, we systematically summarize the cross-talk between cellular senescence and inflammation in OA. We begin by focusing on the mechanisms and hallmarks of cellular senescence, summarizing evidence that supports the relationship between cellular senescence and inflammation. We then discuss the mechanisms of interaction between cellular senescence and inflammation, including senescence-associated secretory phenotypes (SASP) and the effects of pro- and anti-inflammatory interventions on cellular senescence. Additionally, we focus on various types of cellular senescence in OA, including senescence in cartilage, subchondral bone, synovium, infrapatellar fat pad, stem cells, and immune cells, elucidating their mechanisms and impacts on OA. Finally, we highlight the potential of therapies targeting senescent cells in OA as a strategy for promoting cartilage regeneration.
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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.