Evidence map›Paper›PMID 34612510›Full record

ReviewJournal of cellular physiology2022

The broad pathogenetic role of TCF7L2 in human diseases beyond type 2 diabetes.

Laura Del Bosque-Plata, Eduardo Pavel Hernández-Cortés, Claudia Gragnoli

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of cellular physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 6% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Pooled it
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  13. Clinical and Metabolic Signatures ofKidney international reports · 2025
    Article
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  17. International journal of medical sciences · 2025
    Article
  18. A Genetic Clue to T2DM in Bangladesh: TheOman medical journal · 2025
    Article
  19. 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

3 authors at 2 institutions in 3 countries.

Laura Del Bosque-PlataLaboratorio de Nutrigenética y Nutrigenómica, Instituto Nacional de Medicina Genómica, Mexico City, Mexico.ORCID 0000-0003-3224-378X
Eduardo Pavel Hernández-CortésLaboratorio de Nutrigenética y Nutrigenómica, Instituto Nacional de Medicina Genómica, Mexico City, Mexico.
Claudia GragnoliDepartment of Medicine, Division of Endocrinology, Diabetes, and Metabolic Disease, Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania.ORCID 0000-0002-3873-6617
National Institute of Genomic Medicine · MXCreighton University · US

Funding

Genetic Neuro-Endocrine Role in Depression and Type 2 DiabetesR01HD086911 · NICHD · THOMAS JEFFERSON UNIVERSITY · PI GRAGNOLI, CLAUDIA · 2016 to 2020
$1.5M
NICHD NIH HHS 5R01HD086911NICHD NIH HHS R01 HD086911
6 · The paper itself

Abstract

The TCF7L2 protein is a key transcriptional effector of the Wnt/β-catenin signaling pathway, regulating gene expression. It was initially identified in cancer research and embryologic developmental studies. Later, the TCF7L2 gene was linked to type 2 diabetes (T2D), implicating TCF7L2 and Wnt-signaling in metabolic disorders and homeostasis. In fact, TCF7L2-T2D variants confer the greatest relative risk for T2D, unquestionably predicting conversion to T2D in individuals with impaired glucose tolerance. We aim to describe the relevance of TCF7L2 in other human disorders. The TCF7L2-single nucleotide polymorphisms (SNPs) and T2D-risk association have been replicated in numerous follow-up studies, and research has now been performed in several other diseases. In this article, we discuss common TCF7L2-T2D variants within the framework of their association with human diseases. The TCF7L2 functional regions need to be further investigated because the molecular and cellular mechanisms through which TCF7L2 contributes to risk associations with different diseases are still not fully elucidated. In this review, we show the association of common TCF7L2-T2D variants with many types of diseases. However, the role of rare genetic variations in the TCF7L2 gene in distinct diseases and ethnic groups has not been explored, and understanding their impact on specific phenotypes will be of clinical relevance. This offers an excellent opportunity to gain a clearer picture of the role that the TCF7L2 gene plays in the pathophysiology of human diseases. The potential pleiotropic role of TCF7L2 may underlie a possible pathway for comorbidity in human disorders.

Indexed as

Diabetes Mellitus, Type 2Glucose IntoleranceGenetic Predisposition to DiseaseGenotypeHumansPolymorphism, Single NucleotideTranscription Factor 7-Like 2 ProteinTCF7L2 protein, humanTranscription Factor 7-Like 2 ProteincancerCrohn's diseasediabetesTCF7L2 geneWnt-signaling pathway

Identifiers

PMID34612510
PMCPMC9292842
OpenAlexW3202807120

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.