ReviewFrontiers in immunology2026
Inflammaging and osteoarthritis - therapeutic opportunities.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Combined in vitro microcurrent stimulation and celecoxib suppress NF-κB/NLRP3 signaling and cartilage catabolism in human chondrocytes.Immunologic research · 2026Article
- NO-Responsive Oleanolic Acid Self-Assembled Micelles Co-Loaded with BAY 11-7082 for Synergistic Chondroprotection and Anti-Osteoarthritis Therapy.Bioengineering (Basel, Switzerland) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As patients age, cellular senescence results in senescence-associated secretory phenotype (SASP). The SASP results in secretion of pro-inflammatory cytokines, chemokines, and proteases that drive chronic inflammation and cartilage degradation in osteoarthritis (OA). Accumulation of senescent chondrocytes and macrophages activates key signaling pathways such as NF-κB, MAPK/p38, mTOR, AMPK, and JAK/STAT, leading to sustained inflammation and extracellular matrix (ECM) breakdown. Recent studies have identified pharmacological and gene-based approaches that modulate SASP-related pathways. Small molecules such as anakinra, metformin, and rapamycin show potential in reducing inflammation and preserving cartilage, while microRNA modulation and CRISPR/Cas9 editing provide emerging means to regulate SASP factors at the transcriptional level. This review summarizes the molecular mechanisms by which the SASP contributes to OA pathogenesis and highlights novel therapeutic strategies aimed at attenuating inflammation, maintaining cartilage integrity, and mitigating disease progression.
Indexed as
Identifiers
What 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.