Evidence map›Paper›PMID 18776137›Full record

ArticleDiabetes2008

Lymphocytes from patients with type 1 diabetes display a distinct profile of chromatin histone H3 lysine 9 dimethylation: an epigenetic study in diabetes.

Feng Miao, David D Smith, Lingxiao Zhang, Andrew Min, Wei Feng, Rama Natarajan

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed
8.6field-weighted citation impact, top 2% 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

116 citing papers in PubMed, 249 citations in OpenAlex.

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  8. Lysine acetylation and its role in the pathophysiology of acute pancreatitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  9. Article
  10. Review
  11. Article
  12. Metabolic memory: mechanisms and diseases.Signal transduction and targeted therapy · 2024
    Review
  13. Pathomechanisms of Diabetic Kidney Disease.Journal of clinical medicine · 2023
    Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

56 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Feng MiaoDepartment of Diabetes, Beckman Research Institute of City of Hope, Duarte, CA, USA.
David D Smith
Lingxiao Zhang
Andrew Min
Wei Feng
Rama Natarajan
City of Hope · USBeckman Research Institute

Funding

ZOPOLRESTAT IN NORMOTENSIVE, TYPE 1 DIA WITH INCIPIENT NEPHROPATHYM01RR000043 · NCRR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ZAIA, JOHN A · 1985 to 2010
$76.4M
Inflammatory Gene Transcription In Diabetic ConditionsR01DK065073 · NIDDK · CITY OF HOPE/BECKMAN RESEARCH INSTITUTE · PI NATARAJAN, RAMA · 2003 to 2021
$7.9M
Nuclear Mechanisms of VSMC Gene Regulation and Cellular Interactions in DiabetesR01HL087864 · NHLBI · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI NATARAJAN, RAMA · 2008 to 2012
$2.1M
NCRR NIH HHS M01 RR000043NCRR NIH HHS M01-RR-00043NHLBI NIH HHS R01 HL087864NIDDK NIH HHS R01 DK065073NIDDK NIH HHS R01-DK-065073
6 · The paper itself

Abstract

objectiveThe complexity of interactions between genes and the environment is a major challenge for type 1 diabetes studies. Nuclear chromatin is the interface between genetics and environment and the principal carrier of epigenetic information. Because histone tail modifications in chromatin are linked to gene transcription, we hypothesized that histone methylation patterns in cells from type 1 diabetic patients can provide novel epigenetic insights into type 1 diabetes and its complications. RESEARCH DESIGN AND

methodsWe used chromatin immunoprecipitation (ChIP) linked to microarray (ChIP-chip) approach to compare genome-wide histone H3 lysine 9 dimethylation (H3K9me2) patterns in blood lymphocytes and monocytes from type 1 diabetic patients versus healthy control subjects. Bioinformatics evaluation of methylated candidates was performed by Ingenuity Pathway Analysis (IPA) tools.

resultsA subset of genes in the type 1 diabetic cohort showed significant increase in H3K9me2 in lymphocytes but not in monocytes. CLTA4, a type 1 diabetes susceptibility gene, was one of the candidates displaying increased promoter H3K9me2 in type 1 diabetes. IPA identified two high-scoring networks that encompassed genes showing altered H3K9me2. Many of them were associated with autoimmune and inflammation-related pathways, such as transforming growth factor-beta, nuclear factor-kappaB, p38 mitogen-activated protein kinase, toll-like receptor, and interleukin-6. IPA also revealed biological relationships between these networks and known type 1 diabetes candidate genes.

conclusionsThe concerted and synergistic alteration of histone methylation within the identified network in lymphocytes might have an effect on the etiology of type 1 diabetes and its complications. These studies provide evidence of a novel association between type 1 diabetes and altered histone methylation of key genes that are components of type 1 diabetes-related biological pathways and also a new understanding of the pathology of type 1 diabetes.

Indexed as

AdolescentAdultChildChild, PreschoolChromatinCohort StudiesDiabetes Mellitus, Type 1EnvironmentEpigenesis, GeneticGenetic Predisposition to DiseaseHistonesHumansInsulin-Secreting CellsLymphocytesLysineMiddle AgedChromatinepsilon N-dimethyllysineHistonesLysine

Identifiers

PMID18776137
PMCPMC2584123
OpenAlexW2153835740

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.