Evidence map›Paper›PMID 31796960›Full record

ReviewEndocrinology2020

The Endoplasmic Reticulum and Calcium Homeostasis in Pancreatic Beta Cells.

Irina X Zhang, Malini Raghavan, Leslie S Satin

Abstract readReview
In one paragraph

Review in Endocrinology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
–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

65 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Metabolic Stress Shifts the Function of KArchiv der Pharmazie · 2026
    Article
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5 more citing papers are in PubMed but not listed here.

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.

Irina X ZhangDepartment of Pharmacology and Brehm Diabetes Research Center, University of Michigan, Ann Arbor, MI.
Malini RaghavanDepartment of Microbiology and Immunology Michigan Medicine, University of Michigan, Ann Arbor, MI.
Leslie S SatinDepartment of Pharmacology and Brehm Diabetes Research Center, University of Michigan, Ann Arbor, MI.

Funding

METABOLICALLY-COUPLED ION CHANNEL INTERACTIONS IN ISLETSR01DK046409 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI SATIN, LESLIE S. · 1994 to 2023
$9.1M
Calreticulin-mediated protein folding in health and diseaseR01AI123957 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI RAGHAVAN, MALINI · 2016 to 2025
$3.7M
NIAID NIH HHS R01 AI123957NIDDK NIH HHS R01 DK046409
6 · The paper itself

Abstract

The endoplasmic reticulum (ER) mediates the first steps of protein assembly within the secretory pathway and is the site where protein folding and quality control are initiated. The storage and release of Ca2+ are critical physiological functions of the ER. Disrupted ER homeostasis activates the unfolded protein response (UPR), a pathway which attempts to restore cellular equilibrium in the face of ER stress. Unremitting ER stress, and insufficient compensation for it results in beta-cell apoptosis, a process that has been linked to both type 1 diabetes (T1D) and type 2 diabetes (T2D). Both types are characterized by progressive beta-cell failure and a loss of beta-cell mass, although the underlying causes are different. The reduction of mass occurs secondary to apoptosis in the case of T2D, while beta cells undergo autoimmune destruction in T1D. In this review, we examine recent findings that link the UPR pathway and ER Ca2+ to beta cell dysfunction. We also discuss how UPR activation in beta cells favors cell survival versus apoptosis and death, and how ER protein chaperones are involved in regulating ER Ca2+ levels. Abbreviations: BiP, Binding immunoglobulin Protein ER; endoplasmic reticulum; ERAD, ER-associated protein degradation; IFN, interferon; IL, interleukin; JNK, c-Jun N-terminal kinase; KHE, proton-K+ exchanger; MODY, maturity-onset diabetes of young; PERK, PRKR-like ER kinase; SERCA, Sarco/Endoplasmic Reticulum Ca2+-ATPases; T1D, type 1 diabetes; T2D, type 2 diabetes; TNF, tumor necrosis factor; UPR, unfolded protein response; WRS, Wolcott-Rallison syndrome.

Indexed as

AnimalsApoptosisCalciumCalcium SignalingCell SurvivalDiabetes MellitusEndoplasmic ReticulumHomeostasisHumansInsulin-Secreting CellsPotassiumUnfolded Protein ResponseCalciumPotassiumbeta-cell apoptosisER stress and ER calciumtype 1 diabetestype 2 diabetesUPR

Identifiers

PMID31796960
PMCPMC7028010

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.