Evidence map›Paper›PMID 36982731›Full record

ArticleInternational journal of molecular sciences2023

BCL-XL Overexpression Protects Pancreatic β-Cells against Cytokine- and Palmitate-Induced Apoptosis.

Atenea A Perez-Serna, Reinaldo S Dos Santos, Cristina Ripoll, Angel Nadal, Decio L Eizirik, Laura Marroqui

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

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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

6 authors at 2 institutions in 2 countries.

Atenea A Perez-SernaInstituto de Investigación, Desarrollo e Innovación en Biotecnología Sanitaria de Elche (IDiBE), Universidad Miguel Hernández de Elche, 03202 Elche, Alicante, Spain.ORCID 0000-0002-7594-6365
Reinaldo S Dos SantosInstituto de Investigación, Desarrollo e Innovación en Biotecnología Sanitaria de Elche (IDiBE), Universidad Miguel Hernández de Elche, 03202 Elche, Alicante, Spain.ORCID 0000-0002-3219-4730
Cristina RipollInstituto de Investigación, Desarrollo e Innovación en Biotecnología Sanitaria de Elche (IDiBE), Universidad Miguel Hernández de Elche, 03202 Elche, Alicante, Spain.
Angel NadalInstituto de Investigación, Desarrollo e Innovación en Biotecnología Sanitaria de Elche (IDiBE), Universidad Miguel Hernández de Elche, 03202 Elche, Alicante, Spain.ORCID 0000-0003-4178-2152
Decio L EizirikULB Center for Diabetes Research, Medical Faculty, Université Libre de Bruxelles, 1070 Brussels, Belgium.
Laura MarroquiInstituto de Investigación, Desarrollo e Innovación en Biotecnología Sanitaria de Elche (IDiBE), Universidad Miguel Hernández de Elche, 03202 Elche, Alicante, Spain.ORCID 0000-0003-2931-9317
Universitat de Miguel Hernández d'Elx · ESUniversité Libre de Bruxelles · BE

Funding

The Integrated Stress Response in Human Islets During Early T1DU01DK127786 · NIDDK · UNIVERSITY OF CHICAGO · PI EVANS-MOLINA, CARMELLA, MIRMIRA, RAGHAVENDRA G · 2020 to 2025
$7.1M
Implications of Changes in Islet Exosomal Cargo in Type 1 DiabetesR01DK133881 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI EVANS-MOLINA, CARMELLA, MIRMIRA, RAGHAVENDRA G · 2022 to 2025
$2.7M
iPLA2beta-mediated alternative splicing and -cell death in type 1 diabetesR01DK126444 · NIDDK · UNIVERSITY OF VIRGINIA · PI CHALFANT, CHARLES E., EIZIRIK, DECIO LAKS · 2021 to 2024
$2.0M
NIDDK NIH HHS R01 DK126444NIDDK NIH HHS R01 DK133881NIDDK NIH HHS U01 DK127786
6 · The paper itself

Abstract

Diabetes is a chronic disease that affects glucose metabolism, either by autoimmune-driven β-cell loss or by the progressive loss of β-cell function, due to continued metabolic stresses. Although both α- and β-cells are exposed to the same stressors, such as proinflammatory cytokines and saturated free fatty acids (e.g., palmitate), only α-cells survive. We previously reported that the abundant expression of BCL-XL, an anti-apoptotic member of the BCL-2 family of proteins, is part of the α-cell defense mechanism against palmitate-induced cell death. Here, we investigated whether BCL-XL overexpression could protect β-cells against the apoptosis induced by proinflammatory and metabolic insults. For this purpose, BCL-XL was overexpressed in two β-cell lines-namely, rat insulinoma-derived INS-1E and human insulin-producing EndoC-βH1 cells-using adenoviral vectors. We observed that the BCL-XL overexpression in INS-1E cells was slightly reduced in intracellular Ca

Indexed as

CytokinesInsulin-Secreting CellsAnimalsApoptosisbcl-X ProteinCell LineHumansPalmitatesRatsBCL2L1 protein, humanBcl2l1 protein, ratbcl-X ProteinCytokinesPalmitatesapoptosisBCL-XLCa2+ signalingcytokinesinsulin secretionpalmitatepancreatic β-cells

Identifiers

PMID36982731
PMCPMC10056015
OpenAlexW4327621881

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.