Evidence map›Paper›PMID 34338043›Full record

ReviewAmerican journal of physiology. Endocrinology and metabolism2021

β-Cell autophagy in the pathogenesis of type 1 diabetes.

Charanya Muralidharan, Amelia K Linnemann

Open access · hybridAbstract readReview
In one paragraph

Review in American journal of physiology. Endocrinology and metabolism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

20 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Ginsenoside Rg1 Ameliorates Pancreatic Injuries via the AMPK/mTOR Pathway in vivo and in vitro.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023
    Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. 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

2 authors at 1 institution in 1 country.

Charanya MuralidharanDepartment of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana.
Amelia K LinnemannDepartment of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana.ORCID 0000-0001-7356-4876
Indiana University School of Medicine

Funding

Autophagy/antioxidant response coupling in pancreatic beta-cell homeostasis regulationR01DK124380 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI LINNEMANN, AMELIA K · 2021 to 2025
$2.0M
Functional and molecular characterization of the human islet interferon alpha responseR03DK127766 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI LINNEMANN, AMELIA K · 2020 to 2021
$334k
Mechanisms of IL-6 Signaling in Beta-cell Stress ResponseR03DK115990 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI LINNEMANN, AMELIA K · 2018 to 2019
$236k
HHS | National Institutes of Health (NIH) R03DK115990HHS | National Institutes of Health (NIH) R03DK127766NIDDK NIH HHS R01 DK124380NIDDK NIH HHS R03 DK115990NIDDK NIH HHS R03 DK127766
6 · The paper itself

Abstract

Type 1 diabetes is an insulin-dependent, autoimmune disease where the pancreatic β cells are destroyed resulting in hyperglycemia. This multifactorial disease involves multiple environmental and genetic factors, and has no clear etiology. Accumulating evidence suggests that early signaling defects within the β cells may promote a change in the local immune milieu leading to autoimmunity. Therefore, many studies have been focused on intrinsic β-cell mechanisms that aid in the restoration of cellular homeostasis under environmental conditions that cause dysfunction. One of these intrinsic mechanisms to promote homeostasis is autophagy, defects which are clearly linked with β-cell dysfunction in the context of type 2 diabetes. Recent studies have now also pointed towards β-cell autophagy defects in the context of type 1 diabetes. In this perspectives review, we will discuss the evidence supporting a role for β-cell autophagy in the pathogenesis of type 1 diabetes, including a potential role for unconventional secretion of autophagosomes/lysosomes in the changing dialogue between the β cell and immune cells.

Indexed as

AutophagyDiabetes Mellitus, Type 1Insulin-Secreting CellsAnimalsHumansLysosomesautophagylysosometype 1 diabetesβ cell

Identifiers

PMID34338043
PMCPMC8461796
OpenAlexW3188671842

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.