Evidence map›Paper›PMID 39313296›Full record

ArticleLife science alliance2024

Dysfunctional β-cell longevity in diabetes relies on energy conservation and positive epistasis.

Kavit Raval, Neema Jamshidi, Berfin Seyran, Lukasz Salwinski, Raju Pillai, Lixin Yang, Feiyang Ma, Matteo Pellegrini, Juliana Shin, Xia Yang and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Life science alliance, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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

1 citing paper in PubMed.

  1. 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

11 authors.

Kavit RavalHillblom Islet Research Center, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA.ORCID 0000-0003-0086-8312
Neema JamshidiRadiological Sciences, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA.ORCID 0000-0003-3857-9735
Berfin SeyranHillblom Islet Research Center, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA.ORCID 0009-0001-1346-5769
Lukasz SalwinskiMolecular Cell and Developmental Biology, College of Life Sciences, University of California Los Angeles, Los Angeles, CA, USA.ORCID 0000-0003-4522-1969
Raju PillaiDepartment of Pathology, City-of-Hope, Duarte, CA, USA.
Lixin YangDepartment of Pathology, City-of-Hope, Duarte, CA, USA.ORCID 0000-0002-9429-6580
Feiyang MaMolecular Cell and Developmental Biology, College of Life Sciences, University of California Los Angeles, Los Angeles, CA, USA.
Matteo PellegriniMolecular Cell and Developmental Biology, College of Life Sciences, University of California Los Angeles, Los Angeles, CA, USA.
Juliana ShinDepartment of Molecular and Medical Pharmacology, University of California Los Angeles, Los Angeles, CA, USA.
Xia YangDepartment of Molecular and Medical Pharmacology, University of California Los Angeles, Los Angeles, CA, USA.
Slavica TudzarovaHillblom Islet Research Center, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA STudzarova@mednet.ucla.edu.ORCID 0000-0002-9617-3779

Funding

The Human Pancreas Analysis Program for Type 2 DiabetesU01DK123594 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI Robert Babak Faryabi, KLAUS H KAESTNER · 2019 to 2026
$25.0M
Penn integrated Human Pancreas procurement and Analysis ProgramUC4DK112217 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI BETTS, MICHAEL R, FELDMAN, MICHAEL D · 2016 to 2020
$17.8M
Supplement to Integrated Program for Human Pancreas Procurement and AnalysisUC4DK112232 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI ATKINSON, MARK A., POWERS, ALVIN C · 2016 to 2020
$8.4M
Human Pancreas Analysis Program-T2DU01DK123716 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI ATKINSON, MARK A., BOTTINO, RITA · 2019 to 2024
$6.6M
NIDDK NIH HHS U01 DK123594NIDDK NIH HHS U01 DK123716NIDDK NIH HHS UC4 DK112217NIDDK NIH HHS UC4 DK112232
6 · The paper itself

Abstract

Long-lived PFKFB3-expressing β-cells are dysfunctional partly because of prevailing glycolysis that compromises metabolic coupling of insulin secretion. Their accumulation in type 2 diabetes (T2D) appears to be related to the loss of apoptotic competency of cell fitness competition that maintains islet function by favoring constant selection of healthy "winner" cells. To investigate how PFKFB3 can disguise the competitive traits of dysfunctional "loser" β-cells, we analyzed the overlap between human β-cells with bona fide "loser signature" across diabetes pathologies using the HPAP scRNA-seq and spatial transcriptomics of PFKFB3-positive β-cells from nPOD T2D pancreata. The overlapping transcriptional profile of "loser" β-cells was represented by down-regulated ribosomal biosynthesis and genes encoding for mitochondrial respiration. PFKFB3-positive "loser" β-cells had the reduced expression of HLA class I and II genes. Gene-gene interaction analysis revealed that PFKFB3

Indexed as

Diabetes Mellitus, Type 2Energy MetabolismEpistasis, GeneticInsulin-Secreting CellsPhosphofructokinase-2AnimalsApoptosisHumansMaleMiceMice, Inbred C57BLTranscriptomePFKFB3 protein, humanPhosphofructokinase-2

Identifiers

PMID39313296
PMCPMC11420665

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.