Evidence map›Paper›PMID 25496441›Full record

ArticleEpigenetics2015

Histone acetyltransferase PCAF regulates inflammatory molecules in the development of renal injury.

Jin Huang, Danyang Wan, Jianshuang Li, Hong Chen, Kun Huang, Ling Zheng

Open access · bronzeAbstract read
In one paragraph

Article in Epigenetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
3.6field-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

55 citing papers in PubMed, 118 citations in OpenAlex.

  1. Review
  2. Post‑translational modifications in diabetic kidney disease (Review).International journal of molecular medicine · 2026
    Review
  3. Review
  4. Review
  5. Epigenetic memories induced by hypoxia in AKI-to-CKD transition.Clinical and experimental nephrology · 2025
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Sex-specific epigenetic programming in renal fibrosis and inflammation.American journal of physiology. Renal physiology · 2023
    Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Histone Modifications in Acute Kidney Injury.Kidney diseases (Basel, Switzerland) · 2022
    Review
  20. Article
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

6 authors at 4 institutions in 2 countries.

Jin Huanga College of Life Sciences ; Wuhan University ; Wuhan , Hubei , China.
Danyang Wan
Jianshuang Li
Hong Chen
Kun Huang
Ling Zheng
Huazhong University of Science and Technology · CNWuhan Business University · CNLife University · USWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kidney diseases, including chronic kidney disease (CKD) and acute kidney injury (AKI), are associated with inflammation. The mechanism that regulates inflammation in these renal injuries remains unclear. Here, we demonstrated that p300/CBP-associated factor (PCAF), a histone acetyltransferase, was overexpressed in the kidneys of db/db mice and lipopolysaccharide (LPS)-injected mice. Moreover, elevated histone acetylation, such as H3K18ac, and up-regulation of some inflammatory genes, such as ICAM-1, VCAM-1, and MCP-1, were found upon these renal injuries. Furthermore, increased H3K18ac was recruited to the promoters of ICAM-1, VCAM-1, and MCP-1 in the kidneys of LPS-injected mice. In vitro studies demonstrated that PCAF knockdown in human renal proximal tubule epithelial cells (HK-2) led to downregulation of inflammatory molecules, including VCAM-1, ICAM-1, p50 subunit of NF-κB (p50), and MCP-1 mRNA and protein levels, together with significantly decreased H3K18ac level. Consistent with these, overexpression of PCAF enhanced the expression of inflammatory molecules. Furthermore, PCAF deficiency reduced palmitate-induced recruitment of H3K18ac on the promoters of ICAM-1 and MCP-1, as well as inhibited palmitate-induced upregulation of these inflammatory molecules. In summary, the present work demonstrates that PCAF plays an essential role in the regulation of inflammatory molecules through H3K18ac, which provides a potential therapeutic target for inflammation-related renal diseases.

Indexed as

Acute Kidney InjuryAnimalsCell LineChemokine CCL2FemaleHistonesHumansIntercellular Adhesion Molecule-1MaleMiceMice, Inbred C57BLNF-kappa B p50 Subunitp300-CBP-Associated Factorp300-CBP Transcription FactorsRNA, MessengerVascular Cell Adhesion Molecule-1Ccl2 protein, mouseChemokine CCL2HistonesIcam1 protein, mouseIntercellular Adhesion Molecule-1NF-kappa B p50 Subunitp300-CBP-Associated Factorp300-CBP Transcription FactorsRNA, MessengerVascular Cell Adhesion Molecule-1acute kidney injuryAKI, acute kidney injuryCKD, chronic kidney diseaseCOL4, type IV collagendiabetic nephropathyGNAT, GCN5-related N-acetyltransferasesHATs, histone acetyltransferasesHDACs, histone deacetylaseshistone acetylationsHL, hyperlipidemiaICAM-1, intercellular adhesion molecule-1inflammationLPS, lipopolysaccharideMCP-1, monocyte chemotactic protein 1MnSOD, manganese superoxide dismutaseNF-κB, nuclear factor-κBPCAFPCAF, p300/CBP-associated factorTGFβ-1, transforming growth factor β-1VCAM-1, vascular cell adhesion molecule-1

Identifiers

PMID25496441
PMCPMC4622516
OpenAlexW1967331412

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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.