Activation of FoxO1/ PGC-1α prevents mitochondrial dysfunction and ameliorates mesangial cell injury in diabetic rats

Wu, Lina; Wang, Qingzhu; Guo, Feng; Zhou, Yahui; Ji, Hongfei; Liu, Fei; Ma, Xiaoli; Zhao, Yanyan; Qin, Guijun

doi:10.1016/j.mce.2015.06.007

Cited by 40 publications

(23 citation statements)

References 34 publications

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“…Our results reinforce the importance of mitochondria as one of the key components of this complex and a major part of the multifactorial complications of diabetes (9,10,38,39). This study underscores previous observations by our group and others that improving mitochondrial function, by targeting mitochondrial dynamics, activity, or numbers, is renoprotective in different models of kidney injury, including DN (12,(40)(41)(42)(43)(44)(45)(46)(47)(48). We provide evidence that PGC-1α is a mechanistic target of Tug1 in podocytes in the kidney, through which Tug1 regulates mitochondrial bioenergetics.…”

Section: Methodssupporting

confidence: 88%

Long noncoding RNA Tug1 regulates mitochondrial bioenergetics in diabetic nephropathy

Jiang¹,

Badal²,

et al. 2016

Journal of Clinical Investigation

327

349

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Section: Methodssupporting

confidence: 88%

Long noncoding RNA Tug1 regulates mitochondrial bioenergetics in diabetic nephropathy

Jiang¹,

Badal²,

et al. 2016

Journal of Clinical Investigation

327

349

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show abstract

“…Surprisingly, transgenic mice showed an increased PPARGC1A protein level. It has been revealed that FOXO1 may interact with insulin response sequences on the canonical promoter of the PPARGC1A gene in HepG2 cells, rat kidney mesangial cells, and human skeletal muscle, and thereby up-regulate PPARGC1A expression [ 6 , 10 , 40 ]. These findings may partially explain the physiological role of the intensity-dependent activation of FOXO1 in our study.…”

Section: Discussionmentioning

confidence: 99%

Intensity-dependent gene expression after aerobic exercise in endurance-trained skeletal muscle

Popov

Makhnovskii

Kurochkina

et al. 2018

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We investigated acute exercise-induced gene expression in skeletal muscle adapted to aerobic training. Vastus lateralis muscle samples were taken in ten endurance-trained males prior to, and just after, 4 h, and 8 h after acute cycling sessions with different intensities, 70% and 50% V˙O2max. High-throughput RNA sequencing was applied in samples from two subjects to evaluate differentially expressed genes after intensive exercise (70% V˙O2max), and then the changes in expression for selected genes were validated by quantitative PCR (qPCR). To define exercise-induced genes, we compared gene expression after acute exercise with different intensities, 70% and 50% V˙O2max, by qPCR. The transcriptome is dynamically changed during the first hours of recovery after intensive exercise (70% V˙O2max). A computational approach revealed that the changes might be related to up- and down-regulation of the activity of transcription activators and repressors, respectively. The exercise increased expression of many genes encoding protein kinases, while genes encoding transcriptional regulators were both up- and down-regulated. Evaluation of the gene expression after exercise with different intensities revealed that some genes changed expression in an intensity-dependent manner, but others did not: the majority of genes encoding protein kinases, oxidative phosphorylation and activator protein (AP)-1-related genes significantly correlated with markers of exercise stress (power, blood lactate during exercise and post-exercise blood cortisol), while transcriptional repressors and circadian-related genes did not. Some of the changes in gene expression after exercise seemingly may be modulated by circadian rhythm.

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“…The role of Forkhead box O1 (FOXO1), caused more attention in DN, due to its important role in oxidative stress resistance 8 , 9 . It has been suggested that FOXO1 is closely related to the pathogenesis of DN 10 .…”

Section: Introductionmentioning

confidence: 99%

SIRT1 rs10823108 and FOXO1 rs17446614 responsible for genetic susceptibility to diabetic nephropathy

Zhao

Wei

Hou

et al. 2017

Sci Rep

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SIRT1 and FOXO1 play an important role in the pathogenesis of diabetic nephropathy (DN). However, the association between genetic polymorphisms and susceptibility to type 2 DN (T2DN) has not been explored. In this study, a total of 1066 patients with type 2 diabetes mellitus (T2DM) (413 without and 653 with DN) were enrolled. The genotypes of three htSNPs (rs3818292, rs4746720, rs10823108) within SIRT1 and two htSNPs (rs2721068, rs17446614) in FOXO1 were determined by PCR-RFLP. HbA1C, LDL, HDL, TC, and TG levels were also examined. SIRT1 rs10823108 AA genotype was significantly associated with a decreased risk of DN (OR = 0.60, 95%CI: 0.38–0.97), while GA genotype (OR = 1.77, 95%CI: 1.33–2.35) and AA genotype (OR = 2.32, 95%CI: 1.25–4.34) of FOXO1 rs17446614 was associated with an increased T2DN risk. The interactions among rs1744 6614, BMI and duration of diabetes (OR: 2.63, 95%CI: 1.23–4.31) were also observed. Subsequent haplotype analysis revealed that two haplotype defined by AC (OR: 1.50, 95%CI: 1.15–1.94) and AT (OR: 1.79, 95%CI: 1.06–2.80) within FOXO1 gene may increase the risk of T2DN. In conclusion, genetic variant rs10823108 in SIRT1 and variant rs17446614 in FoxO1 may contribute to the risk of DN in T2DM patients.

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Activation of FoxO1/ PGC-1α prevents mitochondrial dysfunction and ameliorates mesangial cell injury in diabetic rats

Cited by 40 publications

References 34 publications

Long noncoding RNA Tug1 regulates mitochondrial bioenergetics in diabetic nephropathy

Long noncoding RNA Tug1 regulates mitochondrial bioenergetics in diabetic nephropathy

Intensity-dependent gene expression after aerobic exercise in endurance-trained skeletal muscle

SIRT1 rs10823108 and FOXO1 rs17446614 responsible for genetic susceptibility to diabetic nephropathy

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