Lipid accumulation is ahead of epithelial-to-mesenchymal transition and therapeutic intervention by acetyl-CoA carboxylase 2 silence in diabetic nephropathy

Xü, Ying; Huang, Jing; Xin, Wei; Chen, Liyong; Zhao, Xu; Lv, Zhimei; Liu, Yi; Wan, Qiang

doi:10.1016/j.metabol.2014.02.010

Cited by 62 publications

(54 citation statements)

References 36 publications

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“…As reported previously by our group (Xu et al, 2014), high glucose could induce lipid accumulation as well as morphological and phenotypical changes in cultured HK-2 cells, and lipid accumulation was ahead of EMT. Fig.…”

Section: Autophagy Deficiency Exacerbated High-glucose-induced Lipotosupporting

confidence: 83%

“…HK-2 cells, a proximal tubule cell line immortalized by transduction with human papillomavirus type 16 E6/E7 (Cell Culture Center of School of Basic Medicine Peking Union Medical College, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences), were cultured in Dulbecco's MEM (Gibco, USA) containing 10% FBS as described previously (Xu et al, 2014). All cell lines were maintained at 37°C in a humidified atmosphere of 5% CO 2 .…”

Section: Cell Culture and Treatmentmentioning

confidence: 99%

“…Our previous studies revealed that lipotoxicity participates in EMT (Xu et al, 2014), suggesting a link between disturbances of lipid metabolism and cell function maintenance in PTECs. As a mechanism that is closely regulated by nutrient sensing, autophagy is related to lipid metabolism in many ways.…”

Section: Introductionmentioning

confidence: 96%

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The renoprotective role of autophagy activation in proximal tubular epithelial cells in diabetic nephropathy

Xü¹,

Liu²,

Xin³

et al. 2015

Journal of Diabetes and its Complications

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Section: Autophagy Deficiency Exacerbated High-glucose-induced Lipotosupporting

confidence: 83%

Section: Cell Culture and Treatmentmentioning

confidence: 99%

See 1 more Smart Citation

The renoprotective role of autophagy activation in proximal tubular epithelial cells in diabetic nephropathy

Xü¹,

Liu²,

Xin³

et al. 2015

Journal of Diabetes and its Complications

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“…In recent years, fatty acid toxicity was reported to play a critical role in T2D-associated renal injury. Moreover, a lack of ACC2 in high-glucose-cultured HK-2 cells resulted in a faster beta oxidation rate, less lipid deposition and malonyl-CoA content [13]. ACC2 can inhibit palmitic acid-induced autophagy, lower lipid accumulation, and restore cell viability [14], suggesting an important role for ACC2 in the development of DN.…”

Section: Lipid Metabolism-related Genesmentioning

confidence: 99%

The Susceptibility Genes in Diabetic Nephropathy

Wei

Xiao

et al. 2018

Kidney Dis

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Background: Diabetes mellitus (DM) poses a severe threat to global public health. Diabetic nephropathy (DN) is one of the most common complications of diabetes and the leading cause of end-stage renal disease (ESRD). Approximately 30–40% of DM patients in the world progress to ESRD, which emphasizes the effect of genetic factors on DN. Family clustering also supports the important role of hereditary factors in DN and ESRD. Therefore, a large number of genetic studies have been carried out to identify susceptibility genes in different diabetic cohorts. Extensive susceptibility genes of DN and ESRD have not been identified until recently. Summary and Key Messages: Some of these associated genes function as pivotal regulators in the pathogenesis of DN, such as those related to glycometabolism and lipid metabolism. However, the functions of most of these genes remain unclear. In this article, we review several susceptibility genes according to their genetic functions to make it easier to determine their exact effect on DN and to provide a better understanding of the advancements from genetic studies. However, several challenges associated with investigating the genetic factors of DN still exist. For instance, it is difficult to determine whether these variants affect the expression of the protein they encode or other cytokines. More efforts should be made to determine how these genes influence the progression of DN. In addition, many results could not be replicated among races, suggesting that the association between genetic polymorphisms and DN is race-specific. Therefore, large, well-designed studies involving more relevant variables and ethnic groups and more relevant functional studies are urgently needed. These studies may be beneficial and retard the progression of DN by early intervention, especially for patients who carry certain risk alleles or genotypes.

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“…To clarify the contribution of FA b-oxidation in PA-induced autophagy, we treated the cells with either ACC2 shRNA lentivirus transfection to suppress ACC2 expression or with a CPTI inhibitor Etomoxir (Et, Sigma), which represents an enhanced or depressed FA b-oxidation respectively [18,22]. The ACC2 knockdown efficiency was evaluated by qPCR and western blotting (Suppl.…”

Section: Autophagy Was Regulated By Fa Oxidationmentioning

confidence: 99%

Acetyl-CoA carboxylase 2 suppression rescues human proximal tubular cells from palmitic acid induced lipotoxicity via autophagy

Xin

Zhao

Liu

et al. 2015

Biochemical and Biophysical Research Communications

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Lipid accumulation is ahead of epithelial-to-mesenchymal transition and therapeutic intervention by acetyl-CoA carboxylase 2 silence in diabetic nephropathy

Cited by 62 publications

References 36 publications

The renoprotective role of autophagy activation in proximal tubular epithelial cells in diabetic nephropathy

The renoprotective role of autophagy activation in proximal tubular epithelial cells in diabetic nephropathy

The Susceptibility Genes in Diabetic Nephropathy

Acetyl-CoA carboxylase 2 suppression rescues human proximal tubular cells from palmitic acid induced lipotoxicity via autophagy

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