Senescence-associated secretory phenotype: the "pathogenic" factor driving orthopedic degenerative diseases and its regulation.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing preclinical mechanisms and therapeutic concepts without systematic review methodology or new human data.
PubMed 42232719 · doi:10.3389/fragi.2026.1818021
What was done
Narrative review synthesizing published literature on the role of the senescence-associated secretory phenotype (SASP) in orthopedic degenerative diseases, specifically osteoarthritis, intervertebral disc degeneration, and osteoporosis. The review categorizes mechanism-to-disease and mechanism-to-therapy relationships and outlines potential interventions including senolytics, senomorphics, autophagy modulation, and gene- or RNA-targeted strategies.
What was found
The abstract reports no quantitative data or effect sizes. It details qualitative mechanisms whereby SASP components (pro-inflammatory cytokines, chemokines, matrix-degrading enzymes, growth factors, and extracellular vesicles) disrupt musculoskeletal homeostasis through sterile inflammation, extracellular matrix catabolism, paracrine senescence, stem/progenitor cell dysfunction, and aberrant neurovascular remodeling.
Why it matters
This review integrates fragmented evidence on cellular senescence across bone and joint disorders, highlighting preclinical interventions and identifying translational challenges such as delivery specificity and biomarker selection.
Limits
The paper is a non-systematic narrative review providing no new primary empirical data or quantitative meta-analysis. Most discussed therapeutic strategies remain in preclinical stages, with clinical efficacy and safety yet to be established in human trials.
Cited by
- supports Senescent cells secrete pro-inflammatory cytokines that cause damage to surrounding healthy cells.