Fig. 2.

Pro- and anti-inflammatory cytokines are critical in POP development and progression in patients and in PFD animal models. IL-1 is upregulated and associated with many immunological cells, including Ns, DCs, and T cells, resulting in immune dysregulation and chronic inflammation in individuals with POP. A large amount of IL-6 defends against POP and induces chronic inflammation. Moreover, the upregulation of IL-10 induces pain and fibrosis during POP. TNF-α and TRAIL induce ECM remodelling and inflammation via the NF-kB and CASP3 pathways. Dysregulation of TGF-β plays dual roles via the Smad pathway and interactions with EGR2 and collagen molecules. These functions minimize ECM disruption and the severity of POP, fibrosis, and inflammation