Evidence map›Paper›PMID 27902771›Full record

ArticlePloS one2016

Piceatannol Attenuates Renal Fibrosis Induced by Unilateral Ureteral Obstruction via Downregulation of Histone Deacetylase 4/5 or p38-MAPK Signaling.

Sin Young Choi, Zhe Hao Piao, Li Jin, Jung Ha Kim, Gwi Ran Kim, Yuhee Ryu, Ming Quan Lin, Hyung-Seok Kim, Hae Jin Kee, Myung Ho Jeong

Abstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
–field-weighted citation impact
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

31 citing papers in PubMed.

  1. Review
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  5. NADCell communication and signaling : CCS · 2024
    Review
  6. Role of Histone Modifications in Kidney Fibrosis.Medicina (Kaunas, Lithuania) · 2024
    Review
  7. Epigenetic Regulation of EMP/EMT-Dependent Fibrosis.International journal of molecular sciences · 2024
    Review
  8. Review
  9. Sex-specific epigenetic programming in renal fibrosis and inflammation.American journal of physiology. Renal physiology · 2023
    Review
  10. Article
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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

10 authors.

Sin Young ChoiHeart Research Center of Chonnam National University Hospital, Gwangju, Republic of Korea.
Zhe Hao PiaoThe Second Hospital of Jilin University, Changchun, China.
Li JinHeart Research Center of Chonnam National University Hospital, Gwangju, Republic of Korea.
Jung Ha KimHeart Research Center of Chonnam National University Hospital, Gwangju, Republic of Korea.
Gwi Ran KimHeart Research Center of Chonnam National University Hospital, Gwangju, Republic of Korea.
Yuhee RyuHeart Research Center of Chonnam National University Hospital, Gwangju, Republic of Korea.
Ming Quan LinHeart Research Center of Chonnam National University Hospital, Gwangju, Republic of Korea.
Hyung-Seok KimHeart Research Center of Chonnam National University Hospital, Gwangju, Republic of Korea.
Hae Jin KeeHeart Research Center of Chonnam National University Hospital, Gwangju, Republic of Korea.
Myung Ho JeongHeart Research Center of Chonnam National University Hospital, Gwangju, Republic of Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Piceatannol, a resveratrol metabolite, is a phenolic compound found in red wine and grapes. We investigated the effect of piceatannol on renal fibrosis and histone deacetylase (HDAC) expression in a mouse model of unilateral ureteral obstruction (UUO). Fibrosis was established by UUO and piceatannol was intraperitoneally injected for 2 weeks. Piceatannol suppressed extracellular matrix (ECM) protein deposition including collagen type I and fibronectin as well as connective tissue growth factor (CTGF) and α-smooth muscle actin (α-SMA) in UUO kidneys. However, the expressions of epithelial-mesenchymal transition (EMT) marker genes, such as N-cadherin and E-cadherin, were not changed in the kidneys after UUO. Masson's trichrome staining and fluorescence immunostaining showed that piceatannol administration attenuated collagen deposition in UUO kidneys. HDAC1, HDAC4, HDAC5, HDAC6, and HDAC10 protein expression was upregulated in UUO kidneys, whereas that of HDAC8 was downregulated. Piceatannol treatment significantly reduced HDAC4 and HDAC5 protein expression. Further, piceatannol attenuated phosphorylation of p38 mitogen-activated protein kinase (p38-MAPK) in UUO kidneys, but not that of transforming growth factor beta1-Smad2/3. These results suggest that class I HDACs and class IIa/b HDACs are involved in renal fibrosis development. Piceatannol may be a beneficial therapeutic agent for treating renal fibrosis via reduction of HDAC4 and HDAC5 protein expression or suppression of the p38-MAPK signaling pathway.

Indexed as

AnimalsBiomarkersDown-RegulationEpithelial-Mesenchymal TransitionExtracellular Matrix ProteinsFibrosisGene Expression Regulation, EnzymologicHistone DeacetylasesKidneyMaleMAP Kinase Signaling SystemMiceMice, Inbred C57BLp38 Mitogen-Activated Protein KinasesStilbenesUreteral Obstruction3,3',4,5'-tetrahydroxystilbeneBiomarkersExtracellular Matrix ProteinsHdac5 protein, mouseHistone Deacetylasesp38 Mitogen-Activated Protein KinasesStilbenes

Identifiers

PMID27902771
PMCPMC5130266

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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.