Abstract
Renal fibrosis commonly leads to glomerulosclerosis and renal interstitial fibrosis and the main pathological basis involves tubular atrophy and the abnormal increase and excessive deposition of extracellular matrix (ECM). Renal fibrosis can progress to chronic kidney disease. Stem cells have multilineage differentiation potential under appropriate conditions and are easy to obtain. At present, there have been some studies showing that stem cells can alleviate the accumulation of ECM and renal fibrosis. However, the sources of stem cells and the types of renal fibrosis or renal fibrosis models used in these studies have differed. In this review, we summarize the pathogenesis (including signaling pathways) of renal fibrosis, and the effect of stem cell therapy on renal fibrosis as described in preclinical and clinical studies. We found that stem cells from various sources have certain effects on improving renal function and alleviating renal fibrosis. However, additional clinical studies should be conducted to confirm this conclusion in the future.
Highlights
Chronic kidney disease (CKD) is a major epidemiological, clinical, and biomedical challenge that has a high prevalence and high mortality
Liu et al [133] injected UC-MSCconditioned medium (CM) (500 μL) via the left renal artery after surgery in ureteral obstruction (UUO) rats, and the results showed that umbilical cord blood mesenchymal stem cells (UC-mesenchymal stem cells (MSCs))-CM decreased reactive oxygen species (ROS), MDA, α-smooth muscle actin (α-SMA), transforming growth factor-β1 (TGFβ1), tumor necrosis factor α (TNF-α), Col-I, apoptosis, and renal interstitial fibrosis and increased GSH, E-cadherin, and proliferating cell nuclear antigen (PCNA)
The occurrence of renal fibrosis may be associated with the TGF-β/Smad, Notch, Hedgehog, Wnt, TNF-α, NFκB, mitogen-activated protein kinase (MAPK), JAK/STAT, PI3K/AKT, and RHO/Rho coil kinase (ROCK) signaling pathways
Summary
Chronic kidney disease (CKD) is a major epidemiological, clinical, and biomedical challenge that has a high prevalence and high mortality. AMSCs can reduce IL-1β, TNF-α, and IL-6 during the treatment of renal interstitial fibrosis and inhibit activation of the TGF-β1/Smad2/3/7 signaling pathway [23]. The results of animal experiments by Lang and Dai [111] showed that BM-MSCs could significantly alleviate renal fibrosis in a diabetic nephropathy rat model, and the mechanism may be associated with the inhibition of the TGF-β1/Smad pathway, decreased PAI-1 protein expression, reduced ECM accumulation, and the balance of the fibrinolytic system. In a transplantation study of autologous AMSCs, Song et al [23] transplanted AMSCs into UUO model rats by tail vein injection and reported that AMSCs decreased MCP-1, TLR4, TNF-α, IL-1β, IL-6, TGF-β1, Smad2/3, α-SMA, fibroblast-specific protein 1 (FSP-1), and FN and inhibited renal fibrosis. Burgos-Silva et al [128] injected AMSCs into FVB mice by intraperitoneal injection to compare the efficacy of AMSCs on acute kidney
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