Evidence map›Paper›PMID 27082896›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2016

HRD1-Mediated IGF-1R Ubiquitination Contributes to Renal Protection of Resveratrol in db/db Mice.

Caifeng Yan, Weifeng Xu, Yujie Huang, Min Li, Yachen Shen, Hui You, Xiubin Liang

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. Polyphenols and ADPKD: A Further Aid from Nature?Life (Basel, Switzerland) · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Caifeng YanDepartment of Endocrinology (C.Y.), Clinical Medical College of Yangzhou University, Yangzhou 225001, Jiangsu, China; Jiangsu Key Laboratory of Xenotransplantation (C.Y., W.X., Y.H., M.L., Y.S., H.Y., X.L.), Department of Pathophysiology, Nanjing Medical University, Nanjing 210029, Jiangsu, China. and Renal Division (W.X.), Zhuji People Hospital, Zhuji 311800, Zhejiang, China.
Weifeng XuDepartment of Endocrinology (C.Y.), Clinical Medical College of Yangzhou University, Yangzhou 225001, Jiangsu, China; Jiangsu Key Laboratory of Xenotransplantation (C.Y., W.X., Y.H., M.L., Y.S., H.Y., X.L.), Department of Pathophysiology, Nanjing Medical University, Nanjing 210029, Jiangsu, China. and Renal Division (W.X.), Zhuji People Hospital, Zhuji 311800, Zhejiang, China.
Yujie HuangDepartment of Endocrinology (C.Y.), Clinical Medical College of Yangzhou University, Yangzhou 225001, Jiangsu, China; Jiangsu Key Laboratory of Xenotransplantation (C.Y., W.X., Y.H., M.L., Y.S., H.Y., X.L.), Department of Pathophysiology, Nanjing Medical University, Nanjing 210029, Jiangsu, China. and Renal Division (W.X.), Zhuji People Hospital, Zhuji 311800, Zhejiang, China.
Min LiDepartment of Endocrinology (C.Y.), Clinical Medical College of Yangzhou University, Yangzhou 225001, Jiangsu, China; Jiangsu Key Laboratory of Xenotransplantation (C.Y., W.X., Y.H., M.L., Y.S., H.Y., X.L.), Department of Pathophysiology, Nanjing Medical University, Nanjing 210029, Jiangsu, China. and Renal Division (W.X.), Zhuji People Hospital, Zhuji 311800, Zhejiang, China.
Yachen ShenDepartment of Endocrinology (C.Y.), Clinical Medical College of Yangzhou University, Yangzhou 225001, Jiangsu, China; Jiangsu Key Laboratory of Xenotransplantation (C.Y., W.X., Y.H., M.L., Y.S., H.Y., X.L.), Department of Pathophysiology, Nanjing Medical University, Nanjing 210029, Jiangsu, China. and Renal Division (W.X.), Zhuji People Hospital, Zhuji 311800, Zhejiang, China.
Hui YouDepartment of Endocrinology (C.Y.), Clinical Medical College of Yangzhou University, Yangzhou 225001, Jiangsu, China; Jiangsu Key Laboratory of Xenotransplantation (C.Y., W.X., Y.H., M.L., Y.S., H.Y., X.L.), Department of Pathophysiology, Nanjing Medical University, Nanjing 210029, Jiangsu, China. and Renal Division (W.X.), Zhuji People Hospital, Zhuji 311800, Zhejiang, China.
Xiubin LiangDepartment of Endocrinology (C.Y.), Clinical Medical College of Yangzhou University, Yangzhou 225001, Jiangsu, China; Jiangsu Key Laboratory of Xenotransplantation (C.Y., W.X., Y.H., M.L., Y.S., H.Y., X.L.), Department of Pathophysiology, Nanjing Medical University, Nanjing 210029, Jiangsu, China. and Renal Division (W.X.), Zhuji People Hospital, Zhuji 311800, Zhejiang, China.
Nanjing Medical University · CNZhuhai People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many studies have provided evidence to demonstrate the beneficial renal effects of resveratrol (RESV) due to its antioxidant character and its capacity for activation of surtuin 1. However, the molecular mechanisms underlying the protective role of RESV against kidney injury are still incompletely understood. The present study used Lepr db/db (db/db) and Lepr db/m (db/m) mice as models to evaluate the effect of RESV on diabetic nephropathy (DN). RESV reduced proteinuria and attenuated the progress of renal fibrosis in db/db mice. Treatment with RESV markedly attenuated the diabetes-induced changes in renal superoxide dismutase copper/zinc, superoxide dismutase manganese, catalase, and malonydialdehyde as well as the renal expression of nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4), α-smooth muscle actin (α-SMA), and E-cadherin in db/db mice. The kidney expression of the IGF-1 receptor (IGF-1R) was increased in db/db mice, but the expression of 3-hydroxy-3-methylglutaryl reductase degradation (HRD1), a ubiquitin E3 ligase, was significantly decreased in the DN model. RESV treatment dramatically decreased IGF-1R and increased HRD1 expressions, consistent with data obtained with HKC-8 cells. HRD1 physically interacted with IGF-1R in HKC-8 cells and liquid chromatography and tandem mass spectrometry (LC-MS/MS) data supported the concept that IGF-1R is one of the HRD1 substrates. HRD1 promoted the IGF-1R ubiquitination for degradation in HKC-8 cells, and the down-regulation of HRD1 reversed the protective effects of RESV in HKC-8 cells. In summary, we have demonstrated that RESV reduces proteinuria and attenuates the progression of renal fibrosis in db/db mice. These protective effects of RESV on DN were associated with the up-regulation of HRD1, induced by RESV, and the promotion of IGF-1R ubiquitination and degradation.

Indexed as

UbiquitinationAnimalsBiomarkersBody WeightCell LineChromatography, LiquidDiabetes Mellitus, ExperimentalDown-RegulationEpithelial-Mesenchymal TransitionHumansKidneyMaleMice, Inbred C57BLOrgan SizeOxidative StressProtective AgentsBiomarkersProtective AgentsReceptor, IGF Type 1ResveratrolRNA, MessengerStilbenesSyvn1 protein, mouseTransforming Growth Factor betaUbiquitin-Protein Ligases

Identifiers

PMID27082896
PMCPMC5414642
OpenAlexW2339088427

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.