Evidence map›Paper›PMID 33349851›Full record

ReviewEndocrinology2021

TGF-β Signaling in Pancreatic Islet β Cell Development and Function.

Ji-Hyun Lee, Ji-Hyeon Lee, Sushil G Rane

Abstract readReview
In one paragraph

Review in Endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

33 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
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  4. Review
  5. Insulin Resistance and Inflammation.International journal of molecular sciences · 2026
    Review
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  7. Article
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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

3 authors.

Ji-Hyun LeeCell Growth and Metabolism Section, Diabetes, Endocrinology & Obesity Branch, National Institutes of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Clinical Research Center, Bethesda, MD, USA.
Ji-Hyeon LeeCell Growth and Metabolism Section, Diabetes, Endocrinology & Obesity Branch, National Institutes of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Clinical Research Center, Bethesda, MD, USA.
Sushil G RaneCell Growth and Metabolism Section, Diabetes, Endocrinology & Obesity Branch, National Institutes of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Clinical Research Center, Bethesda, MD, USA.

Funding

Cell Cycle Regulators in Pancreatic Development and DiseaseZIADK055105 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI RANE, SUSHIL · 2009 to 2025
$8.4M
Transforming Growth Factor Beta Superfamily Signaling in Pancreas BiologyZIADK075073 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI RANE, SUSHIL · 2012 to 2025
$7.0M
Transforming Growth Factor - Beta Superfamily Signaling in Diabetes and ObesityZIADK055106 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI RANE, SUSHIL · 2009 to 2021
$5.7M
Intramural NIH HHS ZIA DK055106Intramural NIH HHS ZIA DK075073
6 · The paper itself

Abstract

Pancreatic islet beta cells (β-cells) synthesize and secrete insulin in response to rising glucose levels and thus are a prime target in both major forms of diabetes. Type 1 diabetes ensues due to autoimmune destruction of β-cells. On the other hand, the prevailing insulin resistance and hyperglycemia in type 2 diabetes (T2D) elicits a compensatory response from β-cells that involves increases in β-cell mass and function. However, the sustained metabolic stress results in β-cell failure, characterized by severe β-cell dysfunction and loss of β-cell mass. Dynamic changes to β-cell mass also occur during pancreatic development that involves extensive growth and morphogenesis. These orchestrated events are triggered by multiple signaling pathways, including those representing the transforming growth factor β (TGF-β) superfamily. TGF-β pathway ligands play important roles during endocrine pancreas development, β-cell proliferation, differentiation, and apoptosis. Furthermore, new findings are suggestive of TGF-β's role in regulation of adult β-cell mass and function. Collectively, these findings support the therapeutic utility of targeting TGF-β in diabetes. Summarizing the role of the various TGF-β pathway ligands in β-cell development, growth and function in normal physiology, and during diabetes pathogenesis is the topic of this mini-review.

Indexed as

AnimalsCell DifferentiationCell ProliferationHumansInsulin-Secreting CellsIslets of LangerhansOrganogenesisSignal TransductionTransforming Growth Factor betaTransforming Growth Factor betadevelopmentdiabetesfunctionisletspancreasTGF-ββ cells

Identifiers

PMID33349851
PMCPMC8240135

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.