Evidence map›Paper›PMID 30150306›Full record

ArticleDiabetes2018

β-Cell DNA Damage Response Promotes Islet Inflammation in Type 1 Diabetes.

Elad Horwitz, Lars Krogvold, Sophia Zhitomirsky, Avital Swisa, Maya Fischman, Tsuria Lax, Tehila Dahan, Noa Hurvitz, Noa Weinberg-Corem, Agnes Klochendler and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
5.4field-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

43 citing papers in PubMed, 58 citations in OpenAlex.

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  18. Epigenetic Regulation of Pancreas Development and Function.Advances in anatomy, embryology, and cell biology · 2024
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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

17 authors at 6 institutions in 4 countries.

Elad HorwitzDepartment of Developmental Biology and Cancer Research, The Hebrew University, Jerusalem, Israel.ORCID 0000-0003-0361-3374
Lars KrogvoldPaediatric Department, Oslo University Hospital HF, Faculty of Medicine, University of Oslo, Oslo, Norway.
Sophia ZhitomirskyDepartment of Developmental Biology and Cancer Research, The Hebrew University, Jerusalem, Israel.
Avital SwisaDepartment of Developmental Biology and Cancer Research, The Hebrew University, Jerusalem, Israel.
Maya FischmanDepartment of Developmental Biology and Cancer Research, The Hebrew University, Jerusalem, Israel.
Tsuria LaxDepartment of Developmental Biology and Cancer Research, The Hebrew University, Jerusalem, Israel.
Tehila DahanDepartment of Developmental Biology and Cancer Research, The Hebrew University, Jerusalem, Israel.
Noa HurvitzDepartment of Developmental Biology and Cancer Research, The Hebrew University, Jerusalem, Israel.
Noa Weinberg-CoremDepartment of Developmental Biology and Cancer Research, The Hebrew University, Jerusalem, Israel.
Agnes KlochendlerDepartment of Developmental Biology and Cancer Research, The Hebrew University, Jerusalem, Israel.
Alvin C PowersDivision of Diabetes, Endocrinology, and Metabolism, Department of Medicine, Vanderbilt University Medical Center, and Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN.ORCID 0000-0003-1941-5786
Marcela BrissovaDivision of Diabetes, Endocrinology, and Metabolism, Department of Medicine, Vanderbilt University Medical Center, and Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN.
Anne JörnsInstitute of Clinical Biochemistry, Hannover Medical School, Hannover, Germany.
Sigurd LenzenInstitute of Clinical Biochemistry, Hannover Medical School, Hannover, Germany.
Benjamin GlaserEndocrinology and Metabolism Service, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.
Knut Dahl-JørgensenPaediatric Department, Oslo University Hospital HF, Faculty of Medicine, University of Oslo, Oslo, Norway.
Yuval DorDepartment of Developmental Biology and Cancer Research, The Hebrew University, Jerusalem, Israel yuvald@ekmd.huji.ac.il knut.dahl-jorgensen@medisin.uio.no.ORCID 0000-0003-2456-2289
Hebrew University of Jerusalem · ILMedizinische Hochschule Hannover · DEOslo University Hospital · NOHadassah Medical Center · ILVanderbilt University Medical Center · USVA Tennessee Valley Healthcare System · US

Funding

Vanderbilt Diabetes Research CenterP30DK020593 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI OWEN P MCGUINNESS · 2012 to 2026
$29.3M
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
Molecular Mechanisms of Human and Murine Beta Cell Proliferation and RegenerationU01DK089572 · NIDDK · VANDERBILT UNIVERSITY · PI GREINER, DALE LESLIE, HARLAN, DAVID MARSHALL · 2010 to 2014
$8.4M
Discovery of Pancreatic Signatures in Type 2 Diabetes MellitusR24DK106755 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI CAI, LONG, CAPRIOLI, RICHARD M · 2015 to 2019
$6.2M
High-resolution analysis of juvenile human pancreas maturationUC4DK108120 · NIDDK · VANDERBILT UNIVERSITY · PI CAI, LONG, GRADINARU, VIVIANA · 2015 to 2015
$4.4M
Molecular Mechanisms of Physiologic Beta Cell Growth in Juvenile Human PancreasUC4DK104211 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI KIM, SEUNG K, POWERS, ALVIN C · 2014 to 2015
$4.0M
Non-Invasive Diagnosis of Human Beta Cell Damage and DeathUC4DK104216 · NIDDK · UNIVERSITY OF FLORIDA · PI SCHATZ, DESMOND ARTHUR · 2014 to 2014
$1.4M
NIDDK NIH HHS P30 DK020593NIDDK NIH HHS R24 DK106755NIDDK NIH HHS U01 DK089572NIDDK NIH HHS UC4 DK104211NIDDK NIH HHS UC4 DK104216NIDDK NIH HHS UC4 DK108120NIDDK NIH HHS UC4 DK112232
6 · The paper itself

Abstract

Type 1 diabetes (T1D) is an autoimmune disease where pancreatic β-cells are destroyed by islet-infiltrating T cells. Although a role for β-cell defects has been suspected, β-cell abnormalities are difficult to demonstrate. We show a β-cell DNA damage response (DDR), presented by activation of the 53BP1 protein and accumulation of p53, in biopsy and autopsy material from patients with recently diagnosed T1D as well as a rat model of human T1D. The β-cell DDR is more frequent in islets infiltrated by CD45

Indexed as

AdultAnimalsDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1DNA DamageFemaleHumansInflammationInsulin-Secreting CellsIslets of LangerhansMaleMiceMiddle AgedYoung Adult

Identifiers

PMID30150306
PMCPMC6198335
OpenAlexW2889225519

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.