Evidence map›Paper›PMID 34016598›Full record

ReviewDiabetes2021

A Selective Look at Autophagy in Pancreatic β-Cells.

Gemma L Pearson, Morgan A Gingerich, Emily M Walker, Trevor J Biden, Scott A Soleimanpour

Abstract readReview
In one paragraph

Review in Diabetes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Role of Autophagy in Type 2 Diabetes Mellitus: The Metabolic Clash.Journal of cellular and molecular medicine · 2024
    Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Mitochondrial Dynamics and Insulin Secretion.International journal of molecular sciences · 2023
    Review
  16. Article
  17. Article
  18. Review
  19. The Role of Beta Cell Recovery in Type 2 Diabetes Remission.International journal of molecular sciences · 2022
    Review
  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

5 authors.

Gemma L PearsonDepartment of Internal Medicine, University of Michigan, Ann Arbor, MI.
Morgan A GingerichDepartment of Internal Medicine, University of Michigan, Ann Arbor, MI.
Emily M WalkerDepartment of Internal Medicine, University of Michigan, Ann Arbor, MI.
Trevor J BidenGarvan Institute of Medical Research, Sydney, Australia.
Scott A SoleimanpourDepartment of Internal Medicine, University of Michigan, Ann Arbor, MI ssol@med.umich.edu.ORCID 0000-0001-6777-4498

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DAVID P OLSON · 2013 to 2026
$24.3M
SYTEMS AND INTEGRATIVE BIOLOGYT32GM008322 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LOW, MALCOLM JAMES · 1990 to 2020
$5.7M
A Stress-Induced Vicious Cycle In The Development of T1DU01DK127747 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ARVAN, PETER, SATIN, LESLIE S. · 2020 to 2023
$2.8M
Mediators of mitophagy in the regulation of beta cell functionR01DK108921 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SOLEIMANPOUR, SCOTT · 2016 to 2020
$1.9M
Investigating structure-function relationships of disease variants encoded by the diabetes gene Clec16aF31DK122761 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GINGERICH, MORGAN · 2020 to 2021
$85k
Control of beta cell identity by the mitochondrial life cycleI01BX004444 · VA · VETERANS HEALTH ADMINISTRATION · PI SOLEIMANPOUR, SCOTT · 2020 to 2023
–
BLRD VA I01 BX004444NIDDK NIH HHS F31 DK122761NIDDK NIH HHS P30 DK020572NIDDK NIH HHS R01 DK108921NIDDK NIH HHS U01 DK127747NIGMS NIH HHS T32 GM008322
6 · The paper itself

Abstract

Insulin-producing pancreatic β-cells are central to glucose homeostasis, and their failure is a principal driver of diabetes development. To preserve optimal health β-cells must withstand both intrinsic and extrinsic stressors, ranging from inflammation to increased peripheral insulin demand, in addition to maintaining insulin biosynthesis and secretory machinery. Autophagy is increasingly being appreciated as a critical β-cell quality control system vital for glycemic control. Here we focus on the underappreciated, yet crucial, roles for selective and organelle-specific forms of autophagy as mediators of β-cell health. We examine the unique molecular players underlying each distinct form of autophagy in β-cells, including selective autophagy of mitochondria, insulin granules, lipid, intracellular amyloid aggregates, endoplasmic reticulum, and peroxisomes. We also describe how defects in selective autophagy pathways contribute to the development of diabetes. As all forms of autophagy are not the same, a refined view of β-cell selective autophagy may inform new approaches to defend against the various insults leading to β-cell failure in diabetes.

Indexed as

AnimalsAutophagyDiabetes MellitusHumansInsulin-Secreting CellsIslets of LangerhansMitophagyProtein AggregatesTranscription FactorsUbiquitin-Protein Ligasesparkin proteinProtein AggregatesTranscription FactorsUbiquitin-Protein Ligases

Identifiers

PMID34016598
PMCPMC8275885

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.