Progress in anti-fibrosis treatment of chronic kidney disease

doi:10.3969/j.issn.1006-7795.2015.03.001

Abstract

Abstract:

Chronic kidney disease (CKD) is one of the most serious diseases of human being. A lot of researches on the kidney fibrosis, which plays the core role in the progression of CKD, have been conducted recently. Many studies' results indicated that different cells of kidney have different effects on tissue fibrosis and regeneration. Different subgroup of inflammatory cells may actively support the regeneration process. According to these researches, many new methods were developed to treat the kidney fibrosis, including anti-transforming growth factor-β (TGF-β) treatment, anti-oxidative stress, anti-vascular calcification, and anti-chemokines treatments. Mesenchymal stem cells or other cells have been tested for treatment of kidney fibrosis. It will be possible to inhibit, stop, or even reverse kidney fibrosis in the future.

Key words: chronic kidney disease, fibrosis, treatment

CLC Number:

R692

Zhang Dongliang. Progress in anti-fibrosis treatment of chronic kidney disease[J]. Journal of Capital Medical University, 2015, 36(3): 333-337.

0
/ / Recommend

Add to citation manager EndNote|Reference Manager|ProCite|BibTeX|RefWorks

URL: https://journal03.magtech.org.cn/Jweb_sdykdxxb/EN/10.3969/j.issn.1006-7795.2015.03.001

https://journal03.magtech.org.cn/Jweb_sdykdxxb/EN/Y2015/V36/I3/333

References

[1] Jha V, Garcia-Garcia G, Iseki K, et al. Chronic kidney disease: global dimension and perspectives[J]. Lancet,2013,382(9888): 260-272.
[2] Yuen D A, Gilbert R E, Marsden P A. Bone marrow cell therapies for endothelial repair and their relevance to kidney disease[J]. Semin Nephrol,2012,32(2): 215-223.
[3] Siddiqi F S, Advani A. Endothelial-podocyte crosstalk: the missing link between endothelial dysfunction and albuminuria in diabetes[J]. Diabetes,2013,62(11): 3647-3655.
[4] Liapis H, Romagnani P, Anders H J. New insights into the pathology of podocyte loss: mitotic catastrophe[J]. Am J Pathol,2013,185(3): 1364-1374.
[5] Cheung T H, Rando T A. Molecular regulation of stem cell quiescence[J]. Nat Rev Mol Cell Biol,2013, 14(6): 329-340.
[6] Angelotti M L, Ronconi E, Ballerini L, et al. Characterization of renal progenitors committed toward tubular lineage and their regenerative potential in renal tubular injury[J]. Stem Cells,2012, 30(8): 1714-1725.
[7] Kulkarni O P, Hartter I, Mulay S R, et al. Toll-like receptor 4 induced IL22 accelerates kidney regeneration[J]. J Am Soc Nephrol,2014,25(5): 978-989.
[8] Zeisberg M, Kalluri R. Cellular mechanisms of tissue fibrosis. 1. Common and organ-specific mechanisms associated with tissue fibrosis[J]. Am J Physiol Cell Physiol,2013,304(3): C216-C225.
[9] Whaley-Connell A T, Tamura M K, Jurkovitz C T, et al. Advances in CKD detection and determination of prognosis: executive summary of the National Kidney Foundation-Kidney Early Evaluation Program (KEEP) 2012 annual data report[J]. Am J Kidney Dis,2013,61(4 Suppl 2): S1-S3.
[10] Kurts C, Panzer U, Anders H J, et al. The immune system and kidney disease: basic concepts and clinical implications[J]. Nat Rev Immunol,2013,13(10): 738-753.
[11] Ebrahimi B, Eirin A, Li Z, et al. Mesenchymal stem cells improve medullary inflammation and fibrosis after revascularization of swine atherosclerotic renal artery stenosis[J]. PLoS One,2013,8(7): e67474.
[12] Ebrahimi B, Li Z, Eirin A, et al. Addition of endothelial progenitor cells to renal revascularization restores medullary tubular oxygen consumption in swine renal artery stenosis[J]. Am J Physiol Renal Physiol,2012,302(11): F1478-F1485.
[13] Reinders M E, de Fijter J W, Roelofs H, et al. Autologous bone marrow-derived mesenchymal stromal cells for the treatment of allograft rejection after renal transplantation: results of a phase I study[J]. Stem Cells Transl Med,2013,2(2):107-111.
[14] Darisipudi M N, Kulkarni O P, Sayyed S G, et al. Dual blockade of the homeostatic chemokine CXCL12 and the proinflammatory chemokine CCL2 has additive protective effects on diabetic kidney disease[J]. Am J Pathol,2011,179(1): 116-124.
[15] Kaissling B, Lehir M, Kriz W. Renal epithelial injury and fibrosis[J]. Biochim Biophys Acta,2013,1832(7): 931-939.
[16] Pichaiwong W, Hudkins K L, Wietecha T, et al. Reversibility of structural and functional damage in a model of advanced diabetic nephropathy[J]. J Am Soc Nephrol,2013,24(7): 1088-1102.
[17] Williams S J, Zammit S C, Cox A J, et al. 3',4'Bisdifluoromethoxycinnamoylanthranilate (FT061): an orally-active antifibrotic agent that reduces albuminuria in a rat model of progressive diabetic nephropathy[J]. Bioorg Med Chem Lett,2013,23(24): 6868-6873.
[18] Zhong X, Chung A C, Chen H Y, et al. miR-21 is a key therapeutic target for renal injury in a mouse model of type 2 diabetes[J]. Diabetologia,2013,56(3): 663-674.
[19] Putta S, Lanting L, Sun G, et al. Inhibiting microRNA-192 ameliorates renal fibrosis in diabetic nephropathy[J]. J Am Soc Nephrol,2012,23(3): 458-469.
[20] Chai Z, Dai A, Tu Y, et al. Genetic deletion of cell division autoantigen 1 retards diabetes-associated renal injury[J]. J Am Soc Nephrol,2013,24(11): 1782-1792.
[21] Dugan L L, You Y H, Ali S S, et al. AMPK dysregulation promotes diabetes-related reduction of superoxide and mitochondrial function[J]. J Clin Invest,2013,123(11): 4888-4899.
[22] Zhang L N, Xu L, Zhou H Y, et al. Novel small-molecule AMP-activated protein kinase allosteric activator with beneficial effects in db/db mice[J]. PLoS One,2013,8(8): e72092.
[23] Avery L B, Bumpus N N. Valproic acid is a novel activator of AMP-activated protein kinase and decreases liver mass, hepatic fat accumulation, and serum glucose in obese mice[J]. Mol Pharmacol,2014,85(1): 1-10.
[24] Chen J F, Ni H F, Pan M M, et al. Pirfenidone inhibits macrophage infiltration in 5/6 nephrectomized rats[J]. Am J Physiol Renal Physiol,2013,304(6): F676-F685.
[25] Sharma K, Ix J H, Mathew A V, Cho M, et al. Pirfenidone for diabetic nephropathy[J]. J Am Soc Nephrol,2011,22(6): 1144-1151.
[26] Sedeek M, Gutsol A, Montezano A C, et al. Renoprotective effects of a novel Nox1/4 inhibitor in a mouse model of type 2 diabetes[J]. Clin Sci (Lond), 2013,124(3): 191-202.
[27] Gray S P, Di Marco E, Okabe J, et al. NADPH oxidase 1 plays a key role in diabetes mellitus-accelerated atherosclerosis[J]. Circulation,2013,127(18): 1888-1902.
[28] Eid A A, Ford B M, Bhandary B, et al. Mammalian target of rapamycin regulates Nox4-mediated podocyte depletion in diabetic renal injury[J]. Diabetes,2013,62(8): 2935-2947.
[29] Zhou L, Li Y, Zhou D, et al. Loss of Klotho contributes to kidney injury by derepression of Wnt/β-catenin signaling[J]. J Am Soc Nephrol,2013,24(5): 771-785.
[30] Reich B, Schmidbauer K, Rodriguez Gomez M, et al. Fibrocytes develop outside the kidney but contribute to renal fibrosis in a mouse model[J]. Kidney Int,2013,84(1): 78-89.
[31] ChemoCentryx. A study to evaluate the safety and Efficacy of CCX140-B in subjects with diabetic nephropathy[EB/OL].(2014-12-12)[2015-02-03]. http://clinicaltrials.gov/show/NCT01447147 (2013).
[32] Sullivan T, Miao Z, Dairaghi D J, et al. CCR2 antagonist CCX140B provides renal and glycemic benefits in diabetic transgenic human CCR2 knockin mice[J]. Am J Physiol Renal Physiol,2013,305(9): F1288-F1297.
[33] Tan J, Wu W, Xu X, et al. Induction therapy with autologous mesenchymal stem cells in living-related kidney transplants: a randomized controlled trial[J]. JAMA,2012,307(11): 1169-1177.
[34] Coca S G, Singanamala S, Parikh C R. Chronic kidney disease after acute kidney injury: a systematic review and meta-analysis[J]. Kidney Int,2012,81(5): 442-448.