Evidence map›Paper›PMID 27133598›Full record

ReviewJournal of autoimmunity2016

Replicative capacity of β-cells and type 1 diabetes.

Diane Saunders, Alvin C Powers

Open access · greenAbstract readReview
In one paragraph

Review in Journal of autoimmunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
6.0field-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

25 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Pancreatic β-Cell Development and Regeneration.Cold Spring Harbor perspectives in biology · 2022
    Review
  6. Review
  7. Diabetic Kinome Inhibitors-A New Opportunity for β-Cells Restoration.International journal of molecular sciences · 2021
    Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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

2 authors at 2 institutions in 1 country.

Diane SaundersDepartment of Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, TN, United States.
Alvin C PowersDepartment of Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, TN, United States; Division of Diabetes, Endocrinology, and Metabolism, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, United States; VA Tennessee Valley Healthcare System, Nashville, TN, United States. Electronic address: al.powers@vanderbilt.edu.
Vanderbilt University Medical Center · USVA Tennessee Valley Healthcare System · US

Funding

Coordinating Center for Beta Cell Biology ConsortiumU01DK072473 · NIDDK · VANDERBILT UNIVERSITY · PI MAGNUSON, MARK A · 2005 to 2014
$61.0M
Vanderbilt Diabetes Research CenterP30DK020593 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI OWEN P MCGUINNESS · 2012 to 2026
$29.3M
TRANSGENIC MOUSE/ ES CELL SHARES RESOURCESP60DK020593 · NIDDK · VANDERBILT UNIVERSITY · PI MCGUINNESS, OWEN P · 1986 to 2011
$28.1M
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
Multi-Disciplinary Approaches to Driving Therapeutic Human Beta Cell ReplicationU01DK089538 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI STEWART, ANDREW F. · 2010 to 2014
$3.6M
Islet Biology in Cystic Fibrosis Related DiabetesR01DK097829 · NIDDK · PACIFIC NORTHWEST RESEARCH INSTITUTE · PI AGUILAR-BRYAN, LYDIA, POWERS, ALVIN C · 2012 to 2016
$2.9M
Reconstruction of Human Type 1 Diabetes in MiceR24DK092758 · NIDDK · HARVARD UNIVERSITY · PI MELTON, DOUGLAS A · 2011 to 2011
$2.3M
Islet Imaging with Monoclonal AntibodiesR01DK094199 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI LIU, GUOZHENG, POWERS, ALVIN C · 2011 to 2015
$2.1M
GLP-1 to Enhance Islet TransplantationR33DK066636 · NIDDK · VANDERBILT UNIVERSITY · PI POWERS, ALVIN C · 2005 to 2007
$1.5M
BLRD VA I01 BX000666BLRD VA I01 BX002223NIDDK NIH HHS P30 DK020593NIDDK NIH HHS P60 DK020593NIDDK NIH HHS R01 DK068764NIDDK NIH HHS R01 DK069603NIDDK NIH HHS R01 DK094199NIDDK NIH HHS R01 DK097829NIDDK NIH HHS R21 DK062641NIDDK NIH HHS R21 DK063439NIDDK NIH HHS R21 DK066636NIDDK NIH HHS R21 DK068854NIDDK NIH HHS R24 DK092758NIDDK NIH HHS R24 DK106755NIDDK NIH HHS R33 DK066636NIDDK NIH HHS U01 DK072473NIDDK NIH HHS U01 DK089538NIDDK NIH HHS U01 DK089572NIDDK NIH HHS UC4 DK104211NIDDK NIH HHS UC4 DK108120
6 · The paper itself

Abstract

Efforts to restore β-cell number or mass in type 1 diabetes (T1D) must combine an intervention to stimulate proliferation of remaining β-cells and an intervention to mitigate or control the β-cell-directed autoimmunity. This review highlights features of the β-cell, including it being part of a pancreatic islet, a mini-organ that is highly vascularized and highly innervated, and efforts to promote β-cell proliferation. In addition, the β-cell in T1D exists in a microenvironment with interactions and input from other islet cell types, extracellular matrix, vascular endothelial cells, neuronal projections, and immune cells, all of which likely influence the β-cell's capacity for replication. Physiologic β-cell proliferation occurs in human and rodents in the neonatal period and early in life, after which there is an age-dependent decline in β-cell proliferation, and also as part of the β-cell's compensatory response to the metabolic challenges of pregnancy and insulin resistance. This review reviews the molecular pathways involved in this β-cell proliferation and highlights recent work in two areas: 1) Investigators, using high-throughput screening to discover small molecules that promote human β-cell proliferation, are now focusing on the dual-specificity tyrosine-regulated kinase-1a and cell cycle-dependent kinase inhibitors CDKN2C/p18 or CDKN1A/p21as targets of compounds to stimulate adult human β-cell proliferation. 2) Local inflammation, macrophages, and the local β-cell microenvironment promote β-cell proliferation. Future efforts to harness the responsible mechanisms may lead to new approaches to promote β-cell proliferation in T1D.

Indexed as

AnimalsAutoimmunityCell ProliferationCellular MicroenvironmentDiabetes Mellitus, Type 1Energy MetabolismHumansInsulin-Secreting CellsIslets of LangerhansMacrophagesMolecular Targeted TherapyRegenerationSignal TransductionAutoimmuneCell proliferationDiabetesIslet

Identifiers

PMID27133598
PMCPMC4903931
OpenAlexW2343901124

What OpenQuestion holds

Textmetadata
LicenceTDM
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.