Psoriasis May Be Linked to Accelerated Cellular Senescence Through Inflammaging Pathways
Psoriasis may be closely linked to cellular senescence and inflammaging, with emerging evidence suggesting that chronic inflammation and senescence-associated secretory phenotype (SASP) signaling contribute to disease pathogenesis and associated comorbidities, according to a recent review.
Psoriasis affects approximately 1% to 3% of the global population and is increasingly recognized as a systemic inflammatory disorder rather than a disease confined to the skin. In addition to cutaneous manifestations, patients experience numerous comorbidities, impaired quality of life, and reduced life expectancy.
The review highlights the role of chronic immune activation in driving persistent inflammation. According to the authors, “psoriasis is perceived as a systemic disorder associated with a systemic inflammatory condition.” Ongoing immune dysregulation leads to production of multiple pro-inflammatory mediators that sustain inflammatory signaling and may accelerate cellular senescence.
A central focus of the review is SASP, a hypersecretory state adopted by senescent cells. SASP is characterized by the release of numerous inflammatory mediators, including cytokines, chemokines, growth factors, proteases, and soluble receptors. The authors note that “multiple SASP-related mediators are dysregulated in psoriasis,” raising the possibility that some may serve as biomarkers or future therapeutic targets.
The relationship between psoriasis and cellular aging appears complex and potentially bidirectional. One proposed mechanism suggests that chronic inflammation promotes cellular senescence and SASP activation, which then contributes to the immune alterations characteristic of psoriasis. An alternative model proposes that psoriasis-associated immune dysregulation initiates systemic inflammation, which subsequently drives senescence.
The review identifies this process as part of “inflammaging,” defined as a chronic, low-grade inflammatory state associated with enhanced cellular senescence. Because psoriasis, inflammation, and senescence may reinforce one another, the authors suggest that understanding these pathways could have implications beyond skin disease alone.
Reference
Filipek K, Nowowiejska-Purpurowicz J, Flisiak I. Inflammaging and senescence-associated secretory phenotype (SASP) in psoriasis—a narrative review of potential mechanisms and anti-inflammaging strategies. Psoriasis (Auckl). 2026;16:598115. doi:10.2147/PTT.S598115
