Evidence map›Paper›PMID 25446993›Full record

ArticleBiochimica et biophysica acta2015

Novel curcumin analog C66 prevents diabetic nephropathy via JNK pathway with the involvement of p300/CBP-mediated histone acetylation.

Yangwei Wang, Yonggang Wang, Manyu Luo, Hao Wu, Lili Kong, Ying Xin, Wenpeng Cui, Yunjie Zhao, Jingying Wang, Guang Liang and 2 more

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

Article in Biochimica et biophysica acta, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

57 citing papers in PubMed, 114 citations in OpenAlex.

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  8. Epigenetic therapeutics attenuate kidney injury and fibrosis by restoring the expression of epigenetically reprogrammed fibrogenic genes and signaling pathways.European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences · 2025
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  13. Unlocking the mechanistic potential ofJournal of traditional and complementary medicine · 2024
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  14. Sex-specific epigenetic programming in renal fibrosis and inflammation.American journal of physiology. Renal physiology · 2023
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  16. Kidney fibrosis: from mechanisms to therapeutic medicines.Signal transduction and targeted therapy · 2023
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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

12 authors at 3 institutions in 2 countries.

Yangwei WangDepartment of Nephrology, Second Hospital of Jilin University, Changchun, China; Kosair Children's Hospital Research Institute and Department of Pediatrics of University of Louisville, Louisville, KY, USA.
Yonggang WangKosair Children's Hospital Research Institute and Department of Pediatrics of University of Louisville, Louisville, KY, USA; Cardiovascular Center, First Hospital of Jilin University, Changchun, China.
Manyu LuoDepartment of Nephrology, Second Hospital of Jilin University, Changchun, China; Kosair Children's Hospital Research Institute and Department of Pediatrics of University of Louisville, Louisville, KY, USA.
Hao WuDepartment of Nephrology, Second Hospital of Jilin University, Changchun, China; Kosair Children's Hospital Research Institute and Department of Pediatrics of University of Louisville, Louisville, KY, USA.
Lili KongDepartment of Nephrology, Second Hospital of Jilin University, Changchun, China; Kosair Children's Hospital Research Institute and Department of Pediatrics of University of Louisville, Louisville, KY, USA.
Ying XinKosair Children's Hospital Research Institute and Department of Pediatrics of University of Louisville, Louisville, KY, USA; Key Laboratory of Pathobiology, Ministry of Education, Jilin University, Changchun, China.
Wenpeng CuiDepartment of Nephrology, Second Hospital of Jilin University, Changchun, China; Kosair Children's Hospital Research Institute and Department of Pediatrics of University of Louisville, Louisville, KY, USA.
Yunjie ZhaoChemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.
Jingying WangChemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.
Guang LiangChemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.
Lining MiaoDepartment of Nephrology, Second Hospital of Jilin University, Changchun, China. Electronic address: miaolining55@163.com.
Lu CaiKosair Children's Hospital Research Institute and Department of Pediatrics of University of Louisville, Louisville, KY, USA; Department of Radiation Oncology, University of Louisville, Louisville, KY, USA; Department of Pharmacology and Toxicology, University of Louisville, Louisville, KY, USA. Electronic address: l0cai001@louisville.edu.
University of Louisville · USWenzhou Medical University · CNSecond Affiliated Hospital of Jilin University · CN

Funding

Metabolomics study on the preventive mechanisms for LDR on diabetic nephropathyR01DK091338 · NIDDK · UNIVERSITY OF LOUISVILLE · PI CAI, LU · 2013 to 2014
$900k
NIDDK NIH HHS 1R01DK091338-01A1NIDDK NIH HHS R01 DK091338
6 · The paper itself

Abstract

Glomerulosclerosis and interstitial fibrosis represent the key events in development of diabetic nephropathy (DN), with connective tissue growth factor (CTGF), plasminogen activator inhibitor-1 (PAI-1) and fibronectin 1 (FN-1) playing important roles in these pathogenic processes. To investigate whether the plant metabolite curcumin, which exerts epigenetic modulatory properties when applied as a pharmacological agent, may prevent DN via inhibition of the JNK pathway and epigenetic histone acetylation, diabetic and age-matched non-diabetic control mice were administered a 3-month course of curcumin analogue (C66), c-Jun N-terminal kinase inhibitor (JNKi, sp600125), or vehicle alone. At treatment end, half of the mice were sacrificed for analysis and the other half were maintained without treatment for an additional 3 months. Renal JNK phosphorylation was found to be significantly increased in the vehicle-treated diabetic mice, but not the C66- and JNKi-treated diabetic mice, at both the 3-month and 6-month time points. C66 and JNKi treatment also significantly prevented diabetes-induced renal fibrosis and dysfunction. Diabetes-related increases in histone acetylation, histone acetyl transferases' (HATs) activity, and the p300/CBP HAT expression were also significantly attenuated by C66 or JNKi treatment. Chromatin immunoprecipitation assays showed that C66 and JNKi treatments decreased H3-lysine9/14-acetylation (H3K9/14Ac) level and p300/CBP occupancy at the CTGF, PAI-1 and FN-1 gene promoters. Thus, C66 may significantly and persistently prevent renal injury and dysfunction in diabetic mice via down-regulation of diabetes-related JNK activation and consequent suppression of the diabetes-related increases in HAT activity, p300/CBP expression, and histone acetylation.

Indexed as

AcetylationAnimalsChromatin ImmunoprecipitationCurcuminDiabetic NephropathiesHistonesMAP Kinase Kinase 4MiceMice, Inbred C57BLp300-CBP Transcription FactorsReal-Time Polymerase Chain ReactionCurcuminHistonesMAP Kinase Kinase 4p300-CBP Transcription FactorsCurcuminDiabetic nephropathyFibrosisHistone acetylationJNKp300/CBP

Identifiers

PMID25446993
PMCPMC4369325
OpenAlexW1991389049

What OpenQuestion holds

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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.