Stem cell-based cell therapy for glomerulonephritis - PubMed (original) (raw)

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Stem cell-based cell therapy for glomerulonephritis

Meiling Jin et al. Biomed Res Int. 2014.

Abstract

Glomerulonephritis (GN), characterized by immune-mediated inflammatory changes in the glomerular, is a common cause of end stage renal disease. Therapeutic options for glomerulonephritis applicable to all cases mainly include symptomatic treatment and strategies to delay progression. In the attempt to yield innovative interventions fostering the limited capability of regeneration of renal tissue after injury and the uncontrolled pathological process by current treatments, stem cell-based therapy has emerged as novel therapy for its ability to inhibit inflammation and promote regeneration. Many basic and clinical studies have been performed that support the ability of various stem cell populations to ameliorate glomerular injury and improve renal function. However, there is a long way before putting stem cell-based therapy into clinical practice. In the present article, we aim to review works performed with respect to the use of stem cell of different origins in GN, and to discuss the potential mechanism of therapeutic effect and the challenges for clinical application of stem cells.

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Figure 1

Figure 1

Potential mechanisms of therapeutical effect of stem cells on glomerulonephritis (GN). Stem cell-based cell therapy is likely to improve the kidney injury in GN mainly via (trans)differentiation of transplant cells into renal cells and paracrine mechanisms. Paracrine mechanisms include anti-inflammatory and immunomodulatory, antifibrosis, antiapoptosis, oxidative stress inhibition, and maintaining normal structure and regeneration. (IL: interleukin, TNF: tumor necrosis factor, IFN-γ: interferon γ, MCP: monocyte chemotactic protein, PDGF-β: platelet-derived growth factor β, BAFF: B-cell activating factor, CTGF: connective tissue growth factor, TGF-β: transforming growth factor-β, PAI-1: plasminogen activator inhibitor 1, EGF: epithelial growth factor, VEGF: vascular endothelial growth factor, HGF: hepatocyte growth factor, IGF-1: insulin-like growth factor, BMP-7: bone morphogenic protein-7, ROS: reactive oxygen species, RNS: reactive nitrogen species.).

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References

    1. Couser WG. Glomerulonephritis. The Lancet. 1999;353(9163):1509–1515. - PubMed
    1. Tanna A, Tam FW, Pusey CD. B-cell-targeted therapy in adult glomerulonephritis. Expert Opinion on Biological Therapy. 2013;13(12):1691–1706. - PubMed
    1. Couchoud C, Stengel B, Landais P, et al. The renal epidemiology and information network (REIN): a new registry for end-stage renal disease in France. Nephrology Dialysis Transplantation. 2006;21(2):411–418. - PubMed
    1. Trivedi HS, Pang MM, Campbell A, Saab P. Slowing the progression of chronic renal failure: economic benefits and patients’ perspectives. American Journal of Kidney Diseases. 2002;39(4):721–729. - PubMed
    1. Chadban SJ, Atkins RC. Glomerulonephritis. The Lancet. 2005;365(9473):1797–1806. - PubMed

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