Erratum to: Resveratrol prevents renal lipotoxicity and inhibits mesangial cell glucotoxicity in a manner dependent on the AMPK–SIRT1–PGC1α axis in db/db mice

Kim, M. Y.; Lim, Ji Hee; Youn, Ho-Joong; Hong, Young Sun; Yang, Ki Hwa; Park, H. S.; Chung, Sung Kun; Ko, Sun-Hye; Shin, Seok Joon; Choi, Byungjoo; Kim, Hyun Woo; Kim, Y. S.; Lee, J. H.; Chang, Yu Sheng; Park, C. W.

doi:10.1007/s00125-012-2791-y

Cited by 4 publications

(3 citation statements)

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“…Resveratrol is a potent activator of SIRT1, which exerts important biological effects on modulation of inflammation, oxidative stress, and cancer, as well as the regulation of glucose and lipid metabolism. Recently, it was found in a DN animal model that resveratrol exhibited renal protective effects by the reduction of proteinuria and extracellular matrix deposition [10,11]. In the present study, resveratrol was shown to regulate the SIRT1-downstream target genes PGC-1α and Forkhead box O (FOXO) by increasing mitochondrial function in myocardium and skeletal muscle tissues [12,13].…”

Section: Introductionsupporting

confidence: 51%

Resveratrol Reduces Oxidative Stress and Apoptosis in Podocytes via Sir2-Related Enzymes, Sirtuins1 (SIRT1)/Peroxisome Proliferator-Activated Receptor γ Co-Activator 1α (PGC-1α) Axis

Zhang

Chi

Ren³

et al. 2019

Med Sci Monit

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Background PGC-1α can be activated by deacetylation reactions catalyzed by SIRT1. Resveratrol is currently known as a potent activator of SIRT1. However, it is unknown whether the renal-protective effect of resveratrol is further related to activation of the podocyte SIRT1/PGC-1α pathway. Material/Methods High glucose was used to stimulate mouse podocytes. Resveratrol and PGC-1α siRNA transfection were used to perform co-intervention treatments. The protein and mRNA expression levels of SIRT1, PGC-1α, NRF1, and TFAM were detect by immunofluorescence, Western blot analysis, and qRT-PCR in the podocytes, respectively. DCHF-DA and MitoSOX™ staining were used to monitor the total ROS and mitochondrial ROS levels, respectively. The specific activities of complexes I and III were measured using Complex I and III Assay Kits. Mitochondrial membrane potential and cell apoptosis were measured using JC-1 staining and Annexin V-FITC/PI double-staining, respectively. Results We found that high-glucose stimulation results in time-dependent decreases in the expression of SIRT1, PGC-1α, and its downstream genes NRF1 and mitochondrial transcription factor A (TFAM) for mouse podocytes, and increases ROS levels in cells and mitochondria. Moreover, the expression of nephrin was downregulated and the cell apoptotic rate was increased. Resveratrol treatment can improve abnormalities caused by high-glucose stimulation. In addition, it can also reduce the release of mitochondrial cytochrome C and DIABLO proteins to the cytoplasm and increase respiratory chain complex I and III activity and mitochondrial membrane potential. Conclusions Resveratrol can reduce the oxidative damage and apoptosis of podocytes induced by high-glucose stimulation via SIRT1/PGC-1α-mediated mitochondrial protection.

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Section: Introductionsupporting

confidence: 51%

Resveratrol Reduces Oxidative Stress and Apoptosis in Podocytes via Sir2-Related Enzymes, Sirtuins1 (SIRT1)/Peroxisome Proliferator-Activated Receptor γ Co-Activator 1α (PGC-1α) Axis

Zhang

Chi

Ren³

et al. 2019

Med Sci Monit

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“…RSV has previously been shown to protect against renal insufficiency and pathological changes associated with diabetic nephropathy both in vivo and in vitro (18,22,23). However, the mechanisms responsible for these renoprotective effects remain poorly understood.…”

Section: Discussionmentioning

confidence: 99%

“…In relation to diabetic nephropathy, previous reports have indicated that RSV can ameliorate renal insufficiency and pathological changes, as well as prevent high glucose-induced mesangial cell proliferation and glomerular fibronectin expression though multiple signaling pathways under diabetic conditions both in vivo and in vitro . These include the PI3K/Akt, JNK/nuclear factor kappa B (NF-κB) and Akt/NF-κB pathways (18,22,23). However, to the best of our knowledge, it is not known if a direct link exists between p38 MAPK and TGF-β1 in the mechanisms underlying the protective effect of RSV against diabetic nephropathy.…”

Section: Introductionmentioning

confidence: 99%

Resveratrol ameliorates diabetic nephropathy in rats through negative regulation of the p38 MAPK/TGF-β1 pathway

Qiao¹,

Gao

Wang³

et al. 2017

Experimental and Therapeutic Medicine

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Resveratrol (RSV) has been shown to have a renoprotective effect against diabetic nephropathy, but the underlying mechanisms of this have not been fully elucidated. The aim of the current study was to explore the mechanisms responsible for the therapeutic effects of RSV in rat mesangial cells in vitro and in a rat model of diabetic nephropathy. The viability of CRL-2573 rat mesangial cells and their expression levels of p38, phosphorylated (p)-p38, transforming growth factor beta 1 (TGF-β1) and fibronectin were assessed in response to treatment with high glucose, with or without RSV. Diabetic nephropathy was also induced in Sprague-Dawley rats by streptozotocin treatment. At 8 weeks, basic biochemical parameters and histopathological abnormalities as well as the expression of p38, p-p38, TGF-β1 and fibronectin in rat kidneys were compared between control diabetic rats and those treated with 20 mg/kg RSV daily for 4 weeks. In the mesangial cell line, RSV inhibited high glucose-induced increases in cell viability and fibronectin expression by significantly reducing p38 mitogen-activated protein kinase (MAPK) activation and TGF-β1 expression (P<0.05). In diabetic rats, RSV significantly decreased blood glucose, serum creatinine and urinary albumin levels, as well as the kidney weight and ratio of kidney weight/body weight compared with the control group (P<0.05). Moreover, RSV ameliorated renal histological changes and downregulated the expression of p-p38, TGF-β1 and fibronectin in the kidneys of diabetic rats. These data suggested that RSV protected renal tissue from diabetes-induced injury and that this activity may be via inhibition of the p38 MAPK/TGF-β1 signaling pathway.

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Thalidomide decreases high glucose‑induced extracellular matrix protein synthesis in mesangial cells via the AMPK pathway

Zhang

Yuan

et al. 2018

Exp Ther Med

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A previous study demonstrated the renal-protective effect of thalidomide (Thd) in diabetic nephropathy rats through the activation of the adenosine monophosphate-activated protein kinase (AMPK) and inhibition of the nuclear factor κB (NF-κB)/monocyte chemoattractant protein-1 (MCP-1) and transforming growth factor (TGF)-β1/mothers against decapentaplegic homolog signaling pathways. The association between AMPK inactivation and high glucose (HG)-induced meningeal cell (MC) proliferation and extracellular matrix (ECM) accumulation via NF-κB and TGF-β1 signaling remains unknown. The aim of the current study was to demonstrate the effects of Thd on cell proliferation and ECM expression in HG-cultured MCs and the underlying mechanisms. HG-cultured human MCs were treated with Thd. Cell proliferation was measured by MTT assay and quantification of cell proliferation was based on the measurement of bromodeoxyuridine incorporation. The differences in TGF-β1, fibronectin and MCP-1 protein expression levels were detected via ELISA and western blot analysis. The AMPK signaling pathway was also examined by western blot analysis in MCs. Compound C, an AMPK inhibitor and AICAR (5-aminoimidazole-4-carboxamide 1β-D-ribofuranoside), an AMPK agonist, were used to analyze the functional role of AMPK in MCs. Cell proliferation was significantly decreased in HG-cultured MCs following treatment with high concentrations of Thd (100 and 200 µg/ml) for 24 h compared with the HG-cultured MC group. Thd suppressed the inflammatory processes in HG-induced MCs. These effects were partially mediated through the activation of AMPK and inhibition of the NF-κB/MCP-1 signaling pathways. Taken together, these results suggest that Thd may have therapeutic potential in diabetic renal injury via the AMPK signaling pathway.

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Erratum to: Resveratrol prevents renal lipotoxicity and inhibits mesangial cell glucotoxicity in a manner dependent on the AMPK–SIRT1–PGC1α axis in db/db mice

Cited by 4 publications

References 0 publications

Resveratrol Reduces Oxidative Stress and Apoptosis in Podocytes via Sir2-Related Enzymes, Sirtuins1 (SIRT1)/Peroxisome Proliferator-Activated Receptor γ Co-Activator 1α (PGC-1α) Axis

Resveratrol Reduces Oxidative Stress and Apoptosis in Podocytes via Sir2-Related Enzymes, Sirtuins1 (SIRT1)/Peroxisome Proliferator-Activated Receptor γ Co-Activator 1α (PGC-1α) Axis

Resveratrol ameliorates diabetic nephropathy in rats through negative regulation of the p38 MAPK/TGF-β1 pathway

Thalidomide decreases high glucose‑induced extracellular matrix protein synthesis in mesangial cells via the AMPK pathway

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