Evidence map›Paper›PMID 20970496›Full record

ReviewBiochimica et biophysica acta2011

Epigenetics and autosomal dominant polycystic kidney disease.

Xiaogang Li

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.5field-weighted citation impact, top 16% 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

27 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Histone deacetylases and their inhibitors in kidney diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
  3. Review
  4. Histone Deacetylase 6 (HDAC6) in Ciliopathies: Emerging Insights and Therapeutic Implications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Generation of heterozygous PKD1 mutant pigs exhibiting early-onset renal cyst formation.Laboratory investigation; a journal of technical methods and pathology · 2022
    Article
  10. Review
  11. Review
  12. Recent Discoveries in Epigenetic Modifications of Polycystic Kidney Disease.International journal of molecular sciences · 2021
    Review
  13. Review
  14. Review
  15. Inhibition of HDAC6 activity in kidney diseases: a new perspective.Molecular medicine (Cambridge, Mass.) · 2018
    Review
  16. Article
  17. Epigenetics of Renal Development and Disease.The Yale journal of biology and medicine · 2016
    Review
  18. Article
  19. Article
  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

1 author at 1 institution in 1 country.

Xiaogang LiDepartment of Pediatrics and Physiology, Medical College of Wisconsin, Milwaukee, WI53226, USA. xxli@mcw.edu
Medical College of Wisconsin · US

Funding

ADPKD: Understanding mechanisms, Discovering treatments.R01DK084097 · NIDDK · UNIVERSITY OF KANSAS MEDICAL CENTER · PI LI, XIAOGANG · 2010 to 2018
$2.3M
NIDDK NIH HHS R01 DK084097
6 · The paper itself

Abstract

The roles of epigenetic modulation of gene expression and protein functions in autosomal dominant polycystic kidney disease (ADPKD) have recently become the focus of scientific investigation. Evidence generated to date indicates that one of the epigenetic modifiers, histone deacetylases (HDACs), are important regulators of ADPKD. HDACs are involved in regulating the expression of the Pkd1 gene and are the target of fluid flow-induced calcium signal in kidney epithelial cells. Pharmacological inhibition of HDAC activity has been found to reduce the progression of cyst formation and slow the decline of kidney function in Pkd1 conditional knockout mice and Pkd2 knockout mice, respectively, implicating the potential clinical application of HDAC inhibitors on ADPKD. Since the expression of HDAC6 is upregulated in cystic epithelial cells, the potential roles of HDAC6 in regulating cilia resorption and epidermal growth factor receptor (EGFR) trafficking through deacetylating α-tubulin and regulating Wnt signaling through deacetylating β-catenin are also discussed. This article is part of a Special Issue entitled: Polycystic Kidney Disease.

Indexed as

Epigenesis, GeneticAnimalsDisease Models, AnimalHistone Deacetylase InhibitorsHistone DeacetylasesHumansMiceModels, BiologicalPolycystic Kidney, Autosomal DominantSignal TransductionTRPP Cation ChannelsHistone Deacetylase InhibitorsHistone DeacetylasesTRPP Cation Channels

Identifiers

PMID20970496
PMCPMC3413450
OpenAlexW2098708707

What OpenQuestion holds

Textmetadata
LicenceTDM
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.