Evidence map›Paper›PMID 26849944›Full record

ArticleFree radical biology & medicine2016

Up-regulation of Nrf2 is involved in FGF21-mediated fenofibrate protection against type 1 diabetic nephropathy.

Yanli Cheng, Jingjing Zhang, Weiying Guo, Fengsheng Li, Weixia Sun, Jing Chen, Chi Zhang, Xuemian Lu, Yi Tan, Wenke Feng and 4 more

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

Article in Free radical biology & medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

63 citing papers in PubMed, 109 citations in OpenAlex.

  1. Article
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  6. NRF2 Dysregulation and Therapeutic Insights Across Chronic Kidney Diseases.International journal of molecular sciences · 2025
    Review
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3 more citing papers are in PubMed but not listed here.

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

14 authors at 6 institutions in 2 countries.

Yanli ChengThe First Hospital of Jilin University, Changchun 130021, China; The Chinese-American Research Institute for Diabetic Complications, Wenzhou Medical University, Wenzhou 325035, China; Kosair Children's Hospital Research Institute, Department of Pediatrics, University of Louisville, Louisville, KY 40202, USA.
Jingjing ZhangKosair Children's Hospital Research Institute, Department of Pediatrics, University of Louisville, Louisville, KY 40202, USA; Department of Cardiology at the First Hospital of China Medical University, Shenyang 110016, China; Department of Cardiology at the People's Hospital of Liaoning Province, Shenyang 110016, China.
Weiying GuoThe First Hospital of Jilin University, Changchun 130021, China.
Fengsheng LiThe Second Artillery General Hospital, Beijing 100088, China.
Weixia SunThe First Hospital of Jilin University, Changchun 130021, China.
Jing ChenKosair Children's Hospital Research Institute, Department of Pediatrics, University of Louisville, Louisville, KY 40202, USA.
Chi ZhangThe Chinese-American Research Institute for Diabetic Complications, Wenzhou Medical University, Wenzhou 325035, China; The Third Affiliated Hospital of the Wenzhou Medical University, Ruian 325200, China.
Xuemian LuThe Third Affiliated Hospital of the Wenzhou Medical University, Ruian 325200, China.
Yi TanThe Chinese-American Research Institute for Diabetic Complications, Wenzhou Medical University, Wenzhou 325035, China; Kosair Children's Hospital Research Institute, Department of Pediatrics, University of Louisville, Louisville, KY 40202, USA; The Third Affiliated Hospital of the Wenzhou Medical University, Ruian 325200, China; Department of Pharmacology and Toxicology, University of Louisville, Louisville, KY 40202, USA.
Wenke FengDepartment of Pharmacology and Toxicology, University of Louisville, Louisville, KY 40202, USA; Department of Medicine, University of Louisville, Louisville, KY 40202, USA.
Yaowen FuThe First Hospital of Jilin University, Changchun 130021, China.
Gilbert C LiuChild and Adolescent Health Research Design and Support, University of Louisville, Louisville, KY 40204, USA.
Zhonggao XuThe First Hospital of Jilin University, Changchun 130021, China. Electronic address: renalxu@163.com.
Lu CaiThe Chinese-American Research Institute for Diabetic Complications, Wenzhou Medical University, Wenzhou 325035, China; Kosair Children's Hospital Research Institute, Department of Pediatrics, University of Louisville, Louisville, KY 40202, USA; The Third Affiliated Hospital of the Wenzhou Medical University, Ruian 325200, China; Department of Pharmacology and Toxicology, University of Louisville, Louisville, KY 40202, USA. Electronic address: L0cai001@louisville.edu.
First Hospital of Jilin University · CNUniversity of Louisville · USRuian People's Hospital · CNWenzhou Medical University · CNJilin University · CNSecond Artillery General Hospital of Chinese People's Liberation Army · CN

Funding

Metabolomics study on the preventive mechanisms for LDR on diabetic nephropathyR01DK091338 · NIDDK · UNIVERSITY OF LOUISVILLE · PI CAI, LU · 2013 to 2014
$900k
FGF21 and adipose lipolysis in alcoholic fatty liverR21AA022416 · NIAAA · UNIVERSITY OF LOUISVILLE · PI FENG, WENKE · 2014 to 2015
$388k
NIAAA NIH HHS R21 AA022416NIDDK NIH HHS 1R01DK091338-01A1NIDDK NIH HHS R01 DK091338
6 · The paper itself

Abstract

The lipid lowering medication, fenofibrate (FF), is a peroxisome proliferator-activated receptor-alpha (PPARα) agonist, possessing beneficial effects for type 2 diabetic nephropathy (DN). We investigated whether FF can prevent the development of type 1 DN, and the underlying mechanisms. Diabetes was induced by a single intraperitoneal injection of streptozotocin in C57BL/6J mice. Mice were treated with oral gavage of FF at 100mg/kg every other day for 3 and 6 months. Diabetes-induced renal oxidative stress, inflammation, apoptosis, lipid and collagen accumulation, and renal dysfunction were accompanied by significant decrease in PI3K, Akt, and GSK-3β phosphorylation as well as an increase in the nuclear accumulation of Fyn [a negative regulator of nuclear factor (erythroid-derived 2)-like 2 (Nrf2)]. All these adverse effects were significantly attenuated by FF treatment. FF also significantly increased fibroblast growth factor 21 (FGF21) expression and enhanced Nrf2 function in diabetic and non-diabetic kidneys. Moreover, FF-induced amelioration of diabetic renal damage, including the stimulation of PI3K/Akt/GSK-3β/Fyn pathway and the enhancement of Nrf2 function were abolished in FGF21-null mice, confirming the critical role of FGF21 in FF-induced renal protection. These results suggest for the first time that FF prevents the development of DN via up-regulating FGF21 and stimulating PI3K/Akt/GSK-3β/Fyn-mediated activation of the Nrf2 pathway.

Indexed as

AnimalsApoptosisDiabetes ComplicationsDiabetes Mellitus, ExperimentalDiabetic NephropathiesFenofibrateFibroblast Growth FactorsGene Expression RegulationHumansMiceNF-E2-Related Factor 2Oxidative StressPPAR alphaSignal TransductionFenofibratefibroblast growth factor 21Fibroblast Growth FactorsNfe2l2 protein, mouseNF-E2-Related Factor 2PPAR alphaAntioxidantsDiabetic nephropathyFGF21Nrf2Oxidative stressPPARα agonistType 1 diabetes

Identifiers

PMID26849944
PMCPMC7446394
OpenAlexW2265613929

What OpenQuestion holds

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Registered trials

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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.