Evidence map›Paper›PMID 19583814›Full record

ArticleJournal of cellular and molecular medicine2009

Diabetes- and angiotensin II-induced cardiac endoplasmic reticulum stress and cell death: metallothionein protection.

Jiancheng Xu, Guanjun Wang, Yuehui Wang, Qiuju Liu, Wei Xu, Yi Tan, Lu Cai

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

50 citing papers in PubMed, 95 citations in OpenAlex.

  1. Review
  2. Novel impact of metal ion-induced cell death on diabetic cardiomyopathy pathogenesis and therapy.Apoptosis : an international journal on programmed cell death · 2025
    Review
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  18. Mammalian Metallothionein-2A and Oxidative Stress.International journal of molecular sciences · 2016
    Review
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  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

7 authors at 2 institutions in 2 countries.

Jiancheng XuThe First Hospital of the Jilin University, Changchun, China.
Guanjun Wang
Yuehui Wang
Qiuju Liu
Wei Xu
Yi Tan
Lu Cai
University of Louisville · USJilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have shown cardiac protection by metallothionein (MT) in the development of diabetic cardiomyopathy (DCM) via suppression of cardiac cell death in cardiac-specific MT-overexpressing transgenic (MT-TG) mice. The present study was undertaken to define whether diabetes can induce cardiac endoplasmic reticulum (ER) stress and whether MT can prevent cardiac cell death via attenuating ER stress. Diabetes was induced by streptozotocin in both MT-TG and wild-type (WT) mice. Two weeks, and 2 and 5 months after diabetes onset, cardiac ER stress was detected by expression of ER chaperones, and apoptosis was detected by CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP) and cleaved caspase-3 and caspase-12. Cardiac apoptosis in the WT diabetic mice, but not in MT-TG diabetic mice, was significantly increased 2 weeks after diabetes onset. In parallel with apoptotic effect, significant up-regulation of the ER chaperones, including glucose-regulated protein (GRP)78 and GRP94, cleaved ATF6 and phosporylated eIF2alpha, in the hearts of WT, but not MT-TG diabetic mice. Infusion of angiotensin II (Ang II) also significantly induced ER stress and apoptosis in the hearts of WT, but not in MT-TG mice. Direct administration of chemical ER stress activator tunicamycin significantly increased cardiac cell death only in WT mice. Pre-treatment with antioxidants completely prevented Ang II-induced ER stress and apoptosis in the cultured cardiac cells. These results suggest that ER stress exists in the diabetic heart, which may cause the cardiac cell death. MT prevents both diabetes- and Ang II-induced cardiac ER stress and associated cell death most likely via its antioxidant action, which may be responsible for MT's prevention of DCM.

Indexed as

Angiotensin IIAnimalsAntioxidantsCell DeathCells, CulturedCytoprotectionDiabetes Mellitus, ExperimentalEndoplasmic ReticulumHumansMetallothioneinMiceMice, TransgenicMolecular ChaperonesMyocardiumRatsStress, PhysiologicalAngiotensin IIAntioxidantsMetallothioneinMolecular ChaperonesTunicamycin

Identifiers

PMID19583814
PMCPMC3828862
OpenAlexW2029305679

What OpenQuestion holds

Textmetadata
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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.