PMC:7335494 / 19480-20658
Annnotations
{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7335494","sourcedb":"PMC","sourceid":"7335494","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7335494","text":"A hallmark of metabolic diseases is a high NADH/NAD+ ratio, originating from excessive electron supply. This dysregulation results in an altered mitochondrial function and sirtuin-3 (SIRT-3) activity, which result in oxidative stress and distorted fatty acid β-oxidation (Cortes-Rojo et al., 2020). Increased ROS production was shown to induce excessive remodelling of the ECM in a pathological milieu (Nikitovic et al., 2013). Thus, oxidative stress induced by high-glucose levels, in rat glomerular mesangial cells, resulted in an increased deposition of collagen IV and fibronectin, through the involvement of the TXNIP-NLRP3 inflammasome signalling (Wang et al., 2017). Importantly, the remodelling of renal ECM is involved in the progression of diabetic nephropathy, one of the most serious complications of diabetes mellitus. Treatment aimed at downregulating ROS generation, such as the utilization of dihydroquercetin (DHQ), an important natural dihydroflavone, attenuated the activation of NLRP3 inflammasome and the subsequent of increased deposition to ECM of renal fibrosis-associated proteins upon exposure of renal cells to high glucose levels (Ding et al., 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