Evidence map›Paper›PMID 33808310›Full record

ReviewBiomolecules2021

Inherent Beta Cell Dysfunction Contributes to Autoimmune Susceptibility.

Yong Kyung Kim, Lori Sussel, Howard W Davidson

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
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  6. Article
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  9. Review
  10. Redox regulation of mNature cell biology · 2024
    Article
  11. Review
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

3 authors at 1 institution in 1 country.

Yong Kyung KimBarbara Davis Center for Diabetes, University of Colorado Denver Anschutz Medical Campus, Aurora, CO 80045, USA.
Lori SusselBarbara Davis Center for Diabetes, University of Colorado Denver Anschutz Medical Campus, Aurora, CO 80045, USA.ORCID 0000-0003-4672-7304
Howard W DavidsonBarbara Davis Center for Diabetes, University of Colorado Denver Anschutz Medical Campus, Aurora, CO 80045, USA.
University of Colorado Anschutz Medical Campus · US

Funding

Regulation of Pancreatic Islet Cell FateR01DK082590 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI LORI SUSSEL · 2009 to 2026
$7.3M
PTPN2 mutations affect islet beta cell susceptibility in T1DR01DK125360 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI SUSSEL, LORI · 2020 to 2023
$1.7M
Beatson Foundation #2019-006NIDDK NIH HHS R01 DK082590NIDDK NIH HHS R01 DK125360
6 · The paper itself

Abstract

The pancreatic beta cell is a highly specialized cell type whose primary function is to secrete insulin in response to nutrients to maintain glucose homeostasis in the body. As such, the beta cell has developed unique metabolic characteristics to achieve functionality; in healthy beta cells, the majority of glucose-derived carbons are oxidized and enter the mitochondria in the form of pyruvate. The pyruvate is subsequently metabolized to induce mitochondrial ATP and trigger the downstream insulin secretion response. Thus, in beta cells, mitochondria play a pivotal role in regulating glucose stimulated insulin secretion (GSIS). In type 2 diabetes (T2D), mitochondrial impairment has been shown to play an important role in beta cell dysfunction and loss. In type 1 diabetes (T1D), autoimmunity is the primary trigger of beta cell loss; however, there is accumulating evidence that intrinsic mitochondrial defects could contribute to beta cell susceptibility during proinflammatory conditions. Furthermore, there is speculation that dysfunctional mitochondrial responses could contribute to the formation of autoantigens. In this review, we provide an overview of mitochondrial function in the beta cells, and discuss potential mechanisms by which mitochondrial dysfunction may contribute to T1D pathogenesis.

Indexed as

AnimalsAutoimmunityAutophagyCellular SenescenceDiabetes Mellitus, Type 1EpitopesHumansInsulin-Secreting CellsInsulin SecretionMitochondriaMitophagyEpitopesautoimmunitybeta cellmitochondriapancreatic islettype 1 diabetes

Identifiers

PMID33808310
PMCPMC8065553
OpenAlexW3145855858

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.