References
- Beto JA, Bansal VK, Ing TS, et al. Variation in blood sample collection for determination of hemodialysis adequacy. Council on Renal Nutrition National Research Question Collaborative Study Group. Am J Kidney Dis. 1998;31(1):135–141.
- Wendt TM, Tanji N, Guo J, et al. RAGE drives the development of glomerulosclerosis and implicates podocyte activation in the pathogenesis of diabetic nephropathy. Am J Pathol. 2003;162(4):1123–1137.
- Dalla Vestra M, Masiero A, Roiter AM, et al. Is podocyte injury relevant in diabetic nephropathy? Studies in patients with type 2 diabetes. Diabetes. 2003;52(4):1031–1035.
- Haraldsson B, Sorensson J. Why do we not all have proteinuria? An update of our current understanding of the glomerular barrier. News Physiol Sci. 2004;19:7–10.
- Meyer TW, Bennett PH, Nelson RG. Podocyte number predicts long-term urinary albumin excretion in Pima Indians with Type II diabetes and microalbuminuria. Diabetologia. 1999;42(11):1341–1344.
- Shankland SJ. The podocyte’s response to injury: role in proteinuria and glomerulosclerosis. Kidney Int. 2006;69(12):2131–2147.
- Susztak K, Raff AC, Schiffer M, et al. Glucose-induced reactive oxygen species cause apoptosis of podocytes and podocyte depletion at the onset of diabetic nephropathy. Diabetes. 2006;55(1):225–233.
- Tanaka E, Asanuma K, Kim E, et al. Notch2 activation ameliorates nephrosis. Nat Commun. 2014;5:3296.
- Zhou X, Marks PA, Rifkind RA, et al. Cloning and characterization of a histone deacetylase, HDAC9. Proc Natl Acad Sci USA. 2001;98(19):10572–10577.
- Witt O, Deubzer HE, Milde T, et al. HDAC family: what are the cancer relevant targets? Cancer Lett. 2009;277(1):8–21.
- Yacoub R, Lee K, He JC. The role of SIRT1 in diabetic kidney disease. Front Endocrinol. 2014;5:166.
- Noh H, Oh EY, Seo JY, et al. Histone deacetylase-2 is a key regulator of diabetes- and transforming growth factor-beta1-induced renal injury. Am J Physiol Renal Physiol. 2009;297(3):F729–F739.
- Wang X, Liu J, Zhen J, et al. Histone deacetylase 4 selectively contributes to podocyte injury in diabetic nephropathy. Kidney Int. 2014;86(4):712–725.
- Parra M. Class IIa HDACs - new insights into their functions in physiology and pathology. FEBS J. 2015;282(9):1736–1744.
- Martens-Uzunova ES, Böttcher R, Croce CM, et al. Long noncoding RNA in prostate, bladder, and kidney cancer. Eur Urol. 2014;65(6):1140–1151.
- Ribeiro AO, Schoof CRG, Izzotti A, et al. MicroRNAs: modulators of cell identity, and their applications in tissue engineering. Microrna. 2014;3(1):45–53.
- Wysocka A, Cybulski M, Berbeć H, et al. Prognostic value of paraoxonase 1 in patients undergoing coronary artery bypass grafting surgery. Med Sci Monit. 2014;20:594–600.
- Huang S-S, Ding D-F, Chen S, et al. Resveratrol protects podocytes against apoptosis via stimulation of autophagy in a mouse model of diabetic nephropathy. Sci Rep. 2017;7(1):45692.
- Advani A, Huang Q, Thai K, et al. Long-term administration of the histone deacetylase inhibitor vorinostat attenuates renal injury in experimental diabetes through an endothelial nitric oxide synthase-dependent mechanism. Am J Pathol. 2011;178(5):2205–2214.
- Taunton J, Hassig CA, Schreiber SL. A mammalian histone deacetylase related to the yeast transcriptional regulator Rpd3p. Science. 1996;272(5260):408–411.
- Boffa LC, Vidali G, Mann RS, et al. Suppression of histone deacetylation in vivo and in vitro by sodium butyrate. J Biol Chem. 1978;253(10):3364–3366.
- Layden BT, Angueira AR, Brodsky M, et al. Short chain fatty acids and their receptors: new metabolic targets. Transl Res. 2013;161(3):131–140.
- Samuelsson U, Ludvigsson J. The concentrations of short-chain fatty acids and other microflora-associated characteristics in faeces from children with newly diagnosed Type 1 diabetes and control children and their family members. Diabet Med. 2004;21(1):64–67.