Evidence map›Paper›PMID 27878451›Full record

ReviewClinical reviews in allergy & immunology2017

Beyond Genetics: What Causes Type 1 Diabetes.

Zhen Wang, Zhiguo Xie, Qianjin Lu, Christopher Chang, Zhiguang Zhou

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical reviews in allergy & immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
9.9field-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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 104 citations in OpenAlex.

  1. Pooled it
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  11. Assessment of ImmobilizedFoods (Basel, Switzerland) · 2024
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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

5 authors at 2 institutions in 2 countries.

Zhen WangDiabetes Center, 2nd Xiangya Hospital, and Institute of Metabolism and Endocrinology, Key Laboratory of Diabetes Immunology, Ministry of Education, Central South University, 139 Renmin Middle Rd, Changsha, Hunan, 410011, China.
Zhiguo XieDiabetes Center, 2nd Xiangya Hospital, and Institute of Metabolism and Endocrinology, Key Laboratory of Diabetes Immunology, Ministry of Education, Central South University, 139 Renmin Middle Rd, Changsha, Hunan, 410011, China.
Qianjin LuDepartment of Dermatology, 2nd Xiangya Hospital, Central South University, Hunan Key Laboratory of Medical Epigenomics, 139 Renmin Middle Rd, Changsha, Hunan, 410011, China.
Christopher ChangDivision of Rheumatology, Allergy and Clinical Immunology, University of California, Davis, Davis, CA, USA.
Zhiguang ZhouDiabetes Center, 2nd Xiangya Hospital, and Institute of Metabolism and Endocrinology, Key Laboratory of Diabetes Immunology, Ministry of Education, Central South University, 139 Renmin Middle Rd, Changsha, Hunan, 410011, China. zhouzg@hotmail.com.
Central South University · CNUniversity of California, Davis · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 1 diabetes (T1D) is an autoimmune disease resulting from T cell-mediated β cell destruction in the pancreas of genetically susceptible individuals. Extensive familial and population genetic studies uncovered the strong linkage and association between HLA gene variants and T1D. Non-HLA genes have also been associated with T1D, such as INS, CTLA4, and PTPN22. T1D is considered as one of the most heritable common diseases. However, evidence that monozygotic twins have incomplete concordance of disease susceptibility provides convincing proof that environmental factors also play important roles in the pathogenesis of the disease. Environmental factors can induce the alterations of gene expression via epigenetic mechanisms. Epigenetic modifications refer to the alterations in gene expression without changes of the DNA sequence, but instead occur as a result of DNA methylation, histone modifications, and miRNA regulation. Aberrant epigenetic modifications will cause the dysregulation of gene expression, thus leading to a variety of human diseases. There are significant differences in DNA methylation, histone modifications, and miRNA profiling found in T1D patients compared with healthy individuals. Epigenetic modifications contribute to the pathogenesis of T1D mainly by regulating the expression of susceptible genes in T1D. These susceptible genes are involved in antigen presentation (such as HLA), immune tolerance (such as FOXP3 and CTLA4), autoreactive T cell response (such as GAD65), and β cell functions (such as INS). A better understanding of epigenetic mechanisms for regulating susceptible genes of T1D will help identify candidates that target epigenetic pathways to control and/or prevent T1D. Knowledge of epigenetic changes in T1D also provides us with potential biomarkers for diagnosis, prognostication, personalized treatment, and prevention of the disease.

Indexed as

Diabetes Mellitus, Type 1Epigenesis, GeneticGene Expression RegulationGenetic Predisposition to DiseaseHumansDNA methylationEnvironmental factorsEpigeneticsGeneticsHistone modificationsmiRNAType 1 diabetes

Identifiers

PMID27878451
OpenAlexW2554969088

What OpenQuestion holds

Textmetadata
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.