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Abstract
AimsThe present study aimed at exploring the mechanisms behind Klotho regulation in hyperglycemia augmented AKI. In addition, epigenetic ways to restore the Klotho expression in AKI-diabetes comorbidity have been evaluated. Main methodsBilateral ischemia-reperfusion injury (IRI) and chemical hypoxia-reperfusion injury (HRI) were developed in diabetic rats and, NRK52E cells under high glucose conditions respectively, to mimic the AKI condition. Plasma, urine, tubular lysate of the kidney and NRK52E cell lysate were used for biochemical, ELISA, histology, immunoblotting, RT-PCR and RNA interference studies. Key findingsHyperglycemia significantly aggravated IRI/HRI induced AKI as evidenced by biochemical and histological results. We also observed a significant increase in expressions of kidney specific histone deacetylases (HDACs), apoptotic and inflammatory proteins, and decrease in levels of endogenous Klotho, H3K9Ac and H3K27Ac proteins in hyperglycemic IRI/HRI groups. SignificanceDiabetes comorbidity exaggerates AKI, where endogenous Klotho loss could be a potential connecting link. However, kidney-specific HDACs inhibition showed reno-protection via restoring the endogenous Klotho loss and thus prevention of inflammation and apoptosis, which could prove to be a potential therapeutic strategy against diabetes-AKI comorbidity.
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