[1] Gnudi L, Coward R J, Long D A. Diabetic nephropathy:Perspective on novel molecular mechanisms[J]. Trends in Endocrinology and Metabolism, 2016:S1043-2760.
[2] Zhou Y, Zhang X, Guan Y. Human antigen r:A novel therapeutic target for diabetic nephropathy?[J]. Journal of Diabetes, 2015, 7(4):462-464.
[3] Robinson-Rechavi M, Escriva Garcia H, Laudet V. The nuclear receptor superfamily[J]. Journal of Cell Science, 2003, 116(4):585-586.
[4] Mukherjee R, Jow L, Noonan D, et al. Human and rat peroxisome proliferator activated receptors (PPARs) demonstrate similar tissue distribution but different responsiveness to PPAR activators[J]. Journal of Steroid Biochemistry and Molecular Biology, 1994, 51(3/4):157-166.
[5] Bookout A L, Jeong Y, Downes M, et al. Anatomical profiling of nuclear receptor expression reveals a hierarchical transcriptional network[J]. Cell, 2006, 126(4):789-799.
[6] Miglio G, Rosa A C, Rattazzi L, et al. The subtypes of peroxisome proliferator-activated receptors expressed by human podocytes and their role in decreasing podocyte injury[J]. British Journal of Clinical Pharmacology, 2011, 162(1):111-125.
[7] Guan Y, Zhang Y, Davis L, et al. Expression of peroxisome proliferator-activated receptors in urinary tract of rabbits and humans[J]. American Journal of Physiology, 1997, 273(6):F1013-F1022.
[8] Guan Y, Zhang Y, Schneider A, et al. Peroxisome proliferator-activated receptor-gamma activity is associated with renal microvasculature[J]. American Journal of Physiology Renal Physiology, 2001, 281(6):F1036-F1046.
[9] Park C W, Zhang Y, Zhang X, et al. PPARalpha agonist fenofibrate improves diabetic nephropathy in db/db mice[J]. Kidney International, 2006, 69(9):1511-1517.
[10] Calkin A C, Giunti S, Jandeleit-Dahm K A, et al. PPAR-alpha and-gamma agonists attenuate diabetic kidney disease in the apolipoprotein E knockout mouse[J]. Nephrology Dialysis Transplantation, 2006, 21(9):2399-2405.
[11] Chen Y J, Quilley J. Fenofibrate treatment of diabetic rats reduces nitrosative stress, renal cyclooxygenase-2 expression, and enhanced renal prostaglandin release[J]. Journal of Pharmacology and Experimental Therapeutics, 2008, 324(2):658-663.
[12] Park C W, Kim H W, Ko S H, et al. Accelerated diabetic nephropathy in mice lacking the peroxisome proliferator-activated receptor alpha[J]. Diabetes, 2006, 55(4):885-893.
[13] Nagai T, Tomizawa T, Nakajima K, et al. Effect of bezafibrate or pravastatin on serum lipid levels and albuminuria in NIDDM patients[J]. Journal of Atherosclerosis and Thrombosis, 2000, 7(2):91-96.
[14] Sacks F M. After the fenofibrate intervention and event lowering in diabetes (FIELD) study:Implications for fenofibrate[J]. Journal of the American College of Cardiology, 2008, 102(12A):34L-40L.
[15] Ruilope L, Hanefeld M, Lincoff A M, et al. Effects of the dual peroxisome proliferator-activated receptor-α/γ agonist aleglitazar on renal function in patients with stage 3 chronic kidney disease and type 2 diabetes:A Phase Ⅱb, randomized study[J]. BMC Nephrology, 2014, 15:180.
[16] Henry R R, Lincoff A M, Mudaliar S, et al. Effect of the dual peroxisome proliferator-activated receptor-alpha/gamma agonist aleglitazar on risk of cardiovascular disease in patients with type 2 diabetes (SYNCHRONY):A phase Ⅱ, randomised, dose-ranging study[J]. The Lancet, 2009, 374(9684):126-135.
[17] Kiss E, Kränzlin B, Wagenblaβ K, et al. Lipid droplet accumulation is associated with an increase in hyperglycemia-induced renal damage:Prevention by liver X receptors[J]. American Journal of Pathology, 2013, 182(3):727-741.
[18] Tanaka Y, Kume S, Araki S, et al. Fenofibrate, a PPARα agonist, has renoprotective effects in mice by enhancing renal lipolysis[J]. Kidney International, 2011, 79(8):871-882.
[19] Chen L, Zhang J, Zhang Y, et al. Improvement of inflammatory responses associated with NF-kappa B pathway in kidneys from diabetic rats[J]. Inflammation Research, 2008, 57(5):199-204.
[20] Chen L L, Zhang J Y, Wang B P. Renoprotective effects of fenofibrate in diabetic rats are achieved by suppressing kidney plasminogen activator inhibitor-1[J]. Vascular Pharmacology, 2006, 44(5):309-315.
[21] Balakumar P, Reddy J, Singh M. Do resident renal mast cells play a role in the pathogenesis of diabetic nephropathy?[J]. Molecular and Cellular Biochemistry, 2009, 330(1/2):187-192.
[22] Tomizawa A, Hattori Y, Inoue T, et al. Fenofibrate suppresses microvascular inflammation and apoptosis through adenosine monophosphate-activated protein kinase activation[J]. Metabolism, 2011, 60(4):513-522.
[23] Matsushita Y, Ogawa D, Wada J, et al. Activation of peroxisome proliferator-activated receptor delta inhibits streptozotocin-induced diabetic nephropathy through anti-inflammatory mechanisms in mice[J]. Diabetes, 2011, 60(3):960-968.
[24] Lee E Y, Kim G T, Hyun M, et al. Peroxisome proliferator-activated receptor-δ activation ameliorates albuminuria by preventing nephrin loss and restoring podocyte integrity in type 2 diabetes[J]. Nephrology Dialysis Transplantation, 2012, 27(11):4069-4079.
[25] Liang Y J, Jian J H, Liu Y C, et al. Advanced glycatin end products-induced apoptosis attenuated by PPARdelta activation and epigallocatechin gallate through NF-kappaB pathway in human embryonic kidney cells and human mesangial cells[J]. Diabetes-Metabolism Research and Reviews, 2010, 26(5):406-416.
[26] Liang Y J, Chen S A, Jian J H. Peroxisome proliferator-activated receptor delta down regulates the expression of the receptor for advanced gllycation end products and pro-inflammatory cytokines in the kidney of streptozotocin-induced diabetic mice[J]. European Journal of Pharmaceutical Sciences, 2011, 43(1/2):65-70.
[27] Ruan X, Zheng F, Guan Y. PPARs and the kidney in metabolic syndrome[J]. American Journal of Physiology Renal Physiology, 2008, 294(5):F1032-F1047.
[28] Zhang Y, Guan Y. PPAR-gamma agonists and diabetic nephropathy[J]. Current Diabetes Reports, 2005, 5(6):470-475.
[29] Guan Y, Hao C, Cha D R, et al. Thiazolidinediones expand body fluid volume through PPARgamma stimulation of ENaC-mediated renal salt absorption[J]. Nature Medicine, 2005, 11(8):81-86.
[30] Agarwal R. Anti-inflammatory effects of short-term pioglitazone therapy in men with advanced diabetic nephropathy[J]. American Journal of Physiology Renal Physiology, 2006, 290(3):F600-F605.
[31] Pistrosch F, Herbrig K, Kindel B, et al. Rosiglitazone improves glomerular hyperfiltration, renal endothelial dysfunction, and microalbuminuria of incipient diabetic nephropathy in patients[J]. Diabetes, 2005, 54(7):2206-2211.
[32] Sarafidis P A, Lasaridis A N. Actions of peroxisome proliferator-activated receptors-gamma agonists explaining a possible blood pressure-lowering effect[J]. American Journal of Hypertension, 2006, 19(6):646-653.
[33] Carmona M C, Louche K, Nibbelink M, et al. Fenofibrate prevents Rosiglitazone-induced body weight gain in ob/ob mice[J]. International Journal of Obesity (Lond), 2005, 29(7):864-871.
[34] Cha D R, Zhang X, Zhang Y, et al. Peroxisome proliferator activated receptor alpha/gamma dual agonist tesaglitazar attenuates diabetic nephropathy in db/db mice[J]. Diabetes, 2007, 56(8):2036-2045.
[35] Liao J, Soltani Z, Ebenezer P, et al. Tesaglitazar, a dual peroxisome proliferator-activated receptor agonist (PPAR alpha/gamma), improves metabolic abnormalities and reduces renal injury in obese Zucker rats[J]. Nephron Experimental Nephrology, 2010, 114(2):e61-e68.
[36] Vionnet N, Tregouët D, Kazeem G, et al. Analysis of 14 candidate genes for diabetic nephropathy on chromosome 3q in European populations:Strongest evidence for association with a variant in the promoter region of the adiponectin gene[J]. Diabetes, 2006, 55(11):3166-3174.
[37] Sharma K, Ramachandrarao S, Qiu G, et al. Adiponectin regulates albuminuria and podocyte function in mice[J]. Journal of Clinical Investigation, 2008, 118(5):1645-1656.
[38] Hallows K R, Mount P F, Pastor-Soler N M, et al. Role of the energy sensor AMP-activated protein kinase in renal physiology and disease[J]. American Journal of Physiology Renal Physiology, 2010, 298(5):F1067-F1077.
[39] Ohga S, Shikata K, Yozai K, et al. Thiazolidinedione ameliorates renal injury in experimental diabetic rats through anti-inflammatory effects mediated by inhibition of NF-kappaB activation[J]. American Journal of Physiology Renal Physiology, 2007, 292(4):F1141-F1150.
[40] Ohtomo S, Izuhara Y, Takizawa S, et al. Thiazolidinediones provide better renoprotection than insulin in an obese, hypertensive type Ⅱ diabetic rat model[J]. Kidney International, 2007, 72(12):1512-1519.
[41] Flaquer M, Lloberas N, Franquesa M, et al. The combination of sirolimus and rosiglitazone produces a renoprotective effect on diabetic kidney disease in rats[J]. Life Sciences, 2010, 87(5/6):147-153.
[42] Tang S C, Leung J C, Chan L Y, et al. Activation of tubular epithelial cells in diabetic nephropathy and the role of the peroxisome proliferator-activated receptor-gamma agonist[J]. Journal of the American Society of Nephrology, 2006, 17(6):1633-1643.
[43] Fukami K, Ueda S, Yamagishi S, et al. AGEs activate mesangial TGF-beta-Smad signaling via an angiotensin Ⅱ type I receptor interaction[J]. Kidney International, 2004, 66(6):2137-2147.
[44] Matsui T, Yamagishi S, Takeuchi M, et al. Nifedipine inhibits advanced glycation end products (AGEs) and their receptor (RAGE) interaction-mediated proximal tubular cell injury via peroxisome proliferator-activated receptor-gamma activation[J]. Biochemical and Biophysical Research Communications, 2010, 398(2):326-330.
[45] Awazu M, Omori S, Ishikura K, et al. The lack of cyclin kinase inhibitor p27(Kip1) ameliorates progression of diabetic nephropathy[J]. Journal of the American Society of Nephrology, 2003, 14(3):699-708.
[46] Huang J S, Chuang L Y, Guh J Y, et al. Antioxidants attenuate high glucose-induced hypertrophic growth in renal tubular epithelial cells[J]. American Journal of Physiology Renal Physiology, 2007, 293(4):F1072-F1082.
[47] Okada T, Wada J, Hida K, et al. Thiazolidinediones ameliorate diabetic nephropathy via cell cycle-dependent mechanisms[J]. Diabetes, 2006, 55(6):1666-1677.
[48] Yuan Y, Zhang A, Huang S, et al. A PPARgamma agonist inhibits aldosterone-induced mesangial cell proliferation by blocking ROS-dependent EGFR intracellular signaling[J]. American Journal of Physiology Renal Physiology, 2011, 300(2):F393-F402.
[49] Li X, Liu W, Wang Q, et al. Emodin suppresses cell proliferation and fibronectin expression via p38MAPK pathway in rat mesangial cells cultured under high glucose[J]. Molecular and Cellular Endocrinology, 2009, 307(1/2):157-162.
[50] Azab M M, Abdel-Azeez H A, Zanaty M F, et al. Peroxisome proliferator activated receptor γ2 gene Pro12Ala gene polymorphism in type 2 diabetes and its relationship with diabetic nephropathy[J]. Linical Chemistry and Laboratory Medicine, 2014, 60(5):743-749.
[51] Huang J S, Chuang C T, Liu M H, et al. Klotho attenuates high glucose-induced fibronectin and cell hypertrophy via the ERK1/2-p38 kinase signaling pathway in renal interstitial fibroblasts[J]. Molecular and Cellular Endocrinology, 2014, 390(1-2):45-53.
[52] Wójcicka G, Jamroz-Wišniewska A, Horoszewicz K, et al. Liver X receptors (LXRs). Part Ⅰ:Structure, function, regulation of activity, and role in lipid metabolism[J]. Postepy Higieny I Medycyny Doswiadczalnej (Online), 2007, 61:736-759.
[53] Bonnet F, Cooper M E. Potential influence of lipids in diabetic nephropathy:Insights from experimental data and clinical studies[J]. Diabetes Obesity & Metabolism, 2000, 26(4):254-264.
[54] Wu J, Zhang Y, Wang N, et al. Liver X receptor-alpha mediates cholesterol efflux in glomerular mesangial cells[J]. American Journal of Physiology Renal Physiology, 2004, 287(5):F886-F895.
[55] Patel M, Wang X X, Magomedova L, et al. Liver X receptors preserve renal glomerular integrity under normoglycaemia and in diabetes in mice[J]. Diabetologia, 2014, 57(2):435-446.
[56] Tachibana H, Ogawa D, Matsushita Y, et al. Activation of liver X receptor inhibits osteopontin and ameliorates diabetic nephropathy[J]. Journal of the American Society of Nephrology, 2012, 23(11):1835-1846.
[57] Robinson-Rechavi M, Escriva Garcia H, Laudet V. The nuclear receptor superfamily[J]. Journal of Cell Science, 2003, 116(4):585-586.
[58] Makishima M, Okamoto A Y, Repa J J, et al. Identification of a nuclear receptor for bile acids[J]. Science, 1999, 284(5418):1362-1365.
[59] Jiang T, Wang X X, Scherzer P, et al. Farnesoid X receptor modulates renal lipid metabolism, fibrosis, and diabetic nephropathy[J]. Diabetes, 2007, 56(10):2485-2493.
[60] Glastras S J, Wong M G, Chen H, et al. FXR expression is associated with dysregulated glucose and lipid levels in the offspring kidney induced by maternal obesity[J]. Nutrition & Metabolism (Lond), 2015, 12:40.
[61] Zhang Y, Kast-Woelbern H R, Edwards R A. Natural structural variants of the nuclear reeptor farnesoid X receptor affect transcriptional activation[J]. Journal of Biological Chemistry, 2003, 278(1):104-110.
[62] Zhang X, Huang S, Gao M, et al. Farnesoid X receptor (FXR) gene deficiency impairs urine concentration in mice[J]. PNAS, 2014, 111(6):2277-2282.
[63] Zhou B, Feng B, Qin Z, et al. Activation of farnesoid X receptor downregulates visfatin and attenuates diabetic nephrapathy[J]. Molecular and Cellular Endocrinology, 2016, 419:72-82.