Evidence map›Paper›PMID 24520198›Full record

ReviewDiabetes, metabolic syndrome and obesity : targets and therapy2014

Stress and the inflammatory process: a major cause of pancreatic cell death in type 2 diabetes.

Joel Montane, Lisa Cadavez, Anna Novials

Open access · goldAbstract readReview
In one paragraph

Review in Diabetes, metabolic syndrome and obesity : targets and therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 2 pooled it
15.4field-weighted citation impact, top 1% 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

71 citing papers in PubMed, 2 syntheses or guidelines pooled it, 159 citations in OpenAlex.

  1. Pooled it
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  10. Mitochondrial protein MPV17 promotes β-cell apoptosis in diabetogenesis.Clinical science (London, England : 1979) · 2023
    Article
  11. Therapeutic Applications and Effects ofFoods (Basel, Switzerland) · 2023
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Clinical medicine insights. Endocrinology and diabetes · 2023
    Article
  17. Article
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  19. Review
  20. Is type 2 diabetes mellitus another intercellular junction-related disorder?Experimental biology and medicine (Maywood, N.J.) · 2022
    Article

11 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 at 3 institutions in 1 country.

Joel MontaneDiabetes and Obesity Research Laboratory, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Hospital Clínic de Barcelona, Barcelona, Spain; Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Barcelona, Spain.
Lisa CadavezDiabetes and Obesity Research Laboratory, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Hospital Clínic de Barcelona, Barcelona, Spain; Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Barcelona, Spain.
Anna NovialsDiabetes and Obesity Research Laboratory, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Hospital Clínic de Barcelona, Barcelona, Spain; Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Barcelona, Spain.
Centro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas · ESConsorci Institut D'Investigacions Biomediques August Pi I Sunyer · ESUniversitat de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 diabetes (T2D) is a complex metabolic disorder characterized by hyperglycemia in the context of insulin resistance, which precedes insulin deficiency as a result of β-cell failure. Accumulating evidence indicates that β-cell loss in T2D results as a response to the combination of oxidative stress and endoplasmic reticulum (ER) stress. Failure of the ER's adaptive capacity and further activation of the unfolded protein response may trigger macroautophagy (hereafter referred as autophagy) as a process of self-protection and inflammation. Many studies have shown that inflammation plays a very important role in the pathogenesis of T2D. Inflammatory mechanisms and cytokine production activated by stress via the inflammasome may further alter the normal structure of β-cells by inducing pancreatic islet cell apoptosis. Thus, the combination of oxidative and ER stress, together with autophagy insufficiency and inflammation, may contribute to β-cell death or dysfunction in T2D. Therapeutic approaches aimed at ameliorating stress and inflammation may therefore prove to be promising targets for the development of new diabetes treatment methods. Here, we discuss different mechanisms involved in stress and inflammation, and the role of antioxidants, endogenous and chemical chaperones, and autophagic pathways, which may shift the tendency from ER stress and apoptosis toward cell survival. Strategies targeting cell survival can be essential for relieving ER stress and reestablishing homeostasis, which may diminish inflammation and prevent pancreatic β-cell death associated with T2D.

Indexed as

apoptosisautophagychaperonesendoplasmic reticulum stressinflammationunfolded protein response

Identifiers

PMID24520198
PMCPMC3917922
OpenAlexW2001252046

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.