ReviewExperimental gerontology2025
Exploring senescence markers as potential drivers of osteoarthritis pain in aging adults.
Review in Experimental gerontology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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.
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Who cites it
6 citing papers in PubMed.
- The Infrapatellar Fat Pad in Osteoarthritis: From Pathophysiology to a Novel Therapeutic Target.International journal of molecular sciences · 2026Review
- Potential crosstalk between ferroptosis and immunosenescence in osteoarthritis: evidence integration and translational insights from the osteoimmune microenvironment.Frontiers in immunology · 2026Review
- Immunometabolic reprogramming in osteoporosis-osteoarthritis comorbidity: from inflammaging to osteochondral unit degeneration.Frontiers in immunology · 2026Review
- Myofascial pain in older adults: a geroscience-informed framework integrating precision geriatrics and digital therapeutics.Frontiers in aging neuroscience · 2026Review
- Plasma levels and peripheral DNA methylation of IGF-1 and IGF-2 across knee osteoarthritis pain phenotypes in middle-aged and older adults.Neurobiology of pain (Cambridge, Mass.)Article
- Circulating cellular senescence biomarkers in persons with chronic knee osteoarthritis pain: An exploratory study.Molecular painArticle
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Senescent cells (SnCs) contribute to various age-related diseases, such as osteoarthritis (OA), a degenerative joint condition that causes persistent pain and reduces physical functioning in older adults. The pathogenesis of OA includes subchondral bone remodeling, synovial inflammation, and cartilage breakdown. Cellular senescence, particularly the pro-inflammatory senescence-associated secretory phenotype (SASP), may have a pivotal role in the progression of OA. SASP factors could exacerbate OA by releasing inflammatory cytokines, chemokines, and proteases, which sensitize nociceptors and accelerate degenerative joint processes, thereby contributing to the chronic pain experienced by OA patients. This contribution of SASPs in chronic pain may lead to mobility limitations and decreased independence of individuals. Thus, the interplay between SASP-driven inflammation and OA pathogenesis may be critical for understanding knee OA pain and functional impairment in older adults. Here, we aim to discuss the parallels between SASP-driven inflammation and OA pathophysiology, which could identify novel therapeutic targets for improving pain management and treatment outcomes in OA.
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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.