From: Advances in stem cell therapy for peritoneal fibrosis: from mechanisms to therapeutics
Types of SCs | Possible mechanisms | Examples |
---|---|---|
MSCs | Settlement and differentiation | BM-MSCs can differentiate into MCs that participate in peritoneal repair and remodelling [34] |
 | Secretion of cytokines acts on MCs | AD-MSCs release HGF and reduce PF by promoting the migration and proliferation of MCs [35] The secretome and soluble factors from pMSCs have shown a significant decrease in PMC death when exposed to PDS [36] |
 | Secretion of EVs | Exosomes from BM-MSCs carry a series of miRNAs with different functions and effectively prevent PF [37] EVs from AD-MSCs can induce rat PMC proliferation and migration via stimulation of the MAPK–ERK1/2 and PI3K–AKT axes [38] Exosomal lncRNA GAS5 derived from UC-MSCs can alleviate MMT through the Wnt/β-catenin signalling pathway [39] |
 | Immunoregulation | BM-MSCs secrete IL-6, IDO and exosomes that affect M2 macrophage differentiation [40,41,42] AD-MSCs attenuate PF by modulating macrophage polarization via IL-6 [43] Preconditioning of MSCs with serum-free culture conditions, IL-1β, IFN-γ, Leishmania major soluble antigens and melatonin can promote anti-inflammatory properties in peritoneal macrophages and reduce PF [40, 44,45,46] SIRT1-modified MSCs can attenuate inflammation and PF through the TGF-β/Smad3 pathway [47] |
USCs | Secretion of EVs | Exosomes from USCs alleviate tissue fibrosis via regulating miR-301b-3p/TGF-βR1 pathway [48] |
 | Immunoregulation | USCs downregulate the Th1/Th17 immune responses in a PGE2-dependent manner and reduce inflammation [49] |
HSCs | Settlement and differentiation | HSCs that originate from the bone marrow have the ability to transform into MCs for repairing and remodelling the peritoneum [34] |
AFSCs | Immunoregulation | Paracrine factors produced by AFSCs cause M1-M2 macrophage polarization in a cell contact-independent way and exhibit anti-inflammatory properties [50] |