Table 2.
Citation | HDAC Inhibitor Studied | HDAC Classes Inhibited | Experimental Models | Outcome |
---|---|---|---|---|
Noh et al., 2009 [54] | Trichostatin A SK-7041 | Trichostatin A, Class I & II; SK-7041 Class I | STZ-diabetic rats, NRK-52E cells | Trichostatin A decreased proteinuria and extracellular matrix production; SK-7041 decreased matrix protein production in vitro |
Gilbert et al., 2011 [6] | Vorinostat | Classes I & II | STZ-diabetic rats, NRK-52E cells | Vorinostat downregulated EGFR expression and decreased tubule cell proliferation and diabetes-associated kidney growth |
Advani et al., 2011 [5] | Vorinostat | Classes I & II | STZ-diabetic wildtype and eNOS−/− mice | Vorinostat downregulated eNOS and reduced oxidative stress, albuminuria and glomerular matrix production in STZ-diabetic wildtype mice but not STZ-diabetic eNOS−/− mice |
Khan et al., 2015 (1) [63] | Valproate | Classes I & II | STZ-diabetic rats | Valproate decreased tubule injury and renal fibrosis |
Khan et al., 2015 (2) [64] | Valproate | Classes I & II | STZ-diabetic rats | Valproate decreased proteinuria and normalized NF-κB upregulation and autophagy downregulation |
Sun et al., 2016 [65] | Valproate | Classes I & II | STZ-diabetic rats | Valproate decreased proteinuria, glomerular matrix deposition, endoplasmic reticulum stress and programmed cell death |
Khan & Jena, 2014 [66] | Sodium butyrate | Classes I & II | STZ-diabetic rats | Sodium butyrate lowered plasma glucose and NF-κB expression and attenuated kidney injury and matrix deposition |
Dong et al., 2017 [67] | Sodium butyrate | Classes I & II | STZ-diabetic wildtype and Nrf2−/− mice | Sodium butyrate prevented Nrf2 downregulation and attenuated oxidative damage, inflammation, programmed cell death, fibrosis and albuminuria but was ineffective in STZ-Nrf2−/− mice |
eNOS = endothelial nitric oxide synthase; NF-κB = nuclear factor kappa-light-chain-enhancer of activated B cells; Nrf2 = nuclear factor erythroid 2-related factor 2.