Evidence map›Paper›PMID 37524865›Full record

ReviewExperimental & molecular medicine2023

Reversing pancreatic β-cell dedifferentiation in the treatment of type 2 diabetes.

Jinsook Son, Domenico Accili

Open access · goldAbstract readReview
In one paragraph

Review in Experimental & molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
27.9field-weighted citation impact, top 1% 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

62 citing papers in PubMed, 88 citations in OpenAlex.

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  10. Coordinated expression and assembly of BiP, p58Proceedings of the National Academy of Sciences of the United States of America · 2026
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2 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Jinsook SonDepartment of Medicine and Naomi Berrie Diabetes Center, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY, 10032, USA. js4730@cumc.columbia.edu.ORCID http://orcid.org/0000-0002-0836-2626
Domenico AcciliDepartment of Medicine and Naomi Berrie Diabetes Center, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY, 10032, USA.
Columbia University · US

Funding

Translational Biomarker Analytical Core (TBAC)P30DK063608 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Rebecca Anne Haeusler, Utpal Pajvani · 2003 to 2026
$36.7M
TTC39B in obesity and atherosclerosisP01HL087123 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI ACCILI, DOMENICO · 2007 to 2022
$31.2M
ROLE OF FORKHEAD PROTEINS IN INSULIN ACTIONR01DK057539 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI ACCILI, DOMENICO · 2001 to 2024
$10.7M
MECHANISMS OF BETA CELL FAILURER01DK064819 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI ACCILI, DOMENICO · 2003 to 2025
$10.5M
MOUSE MODELS OF INSULIN RESISTANCER01DK058282 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI ACCILI, DOMENICO · 2000 to 2023
$6.2M
MOUSE MODELS OF INSULIN RESISTANCER37DK058282 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI ACCILI, DOMENICO · 2010 to 2019
$4.4M
Genetic and pharmacologic inhibition of ALDH1A3 as a treatment of beta cell failureK01DK134848 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI SON, JINSOOK · 2023 to 2025
$461k
Analysis of beta cell dedifferentiation using scRNA-seq of human T2DF32DK117574 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI SON, JINSOOK · 2018 to 2018
$48k
NHLBI NIH HHS P01 HL087123NIDDK NIH HHS F32 DK117574NIDDK NIH HHS K01 DK134848NIDDK NIH HHS P30 DK063608NIDDK NIH HHS R01 DK057539NIDDK NIH HHS R01 DK058282NIDDK NIH HHS R01 DK064819NIDDK NIH HHS R37 DK058282
6 · The paper itself

Abstract

The maintenance of glucose homeostasis is fundamental for survival and health. Diabetes develops when glucose homeostasis fails. Type 2 diabetes (T2D) is characterized by insulin resistance and pancreatic β-cell failure. The failure of β-cells to compensate for insulin resistance results in hyperglycemia, which in turn drives altered lipid metabolism and β-cell failure. Thus, insulin secretion by pancreatic β-cells is a primary component of glucose homeostasis. Impaired β-cell function and reduced β-cell mass are found in diabetes. Both features stem from a failure to maintain β-cell identity, which causes β-cells to dedifferentiate into nonfunctional endocrine progenitor-like cells or to trans-differentiate into other endocrine cell types. In this regard, one of the key issues in achieving disease modification is how to reestablish β-cell identity. In this review, we focus on the causes and implications of β-cell failure, as well as its potential reversibility as a T2D treatment.

Indexed as

Diabetes Mellitus, Type 2Insulin ResistanceInsulin-Secreting CellsCell DedifferentiationGlucoseHumansInsulinGlucoseInsulin

Identifiers

PMID37524865
PMCPMC10474037
OpenAlexW4385407876

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.