Evidence map›Paper›PMID 34053181›Full record

ArticleJournal of cellular and molecular medicine2021

Cardiac metallothionein overexpression rescues diabetic cardiomyopathy in Akt2-knockout mice.

Shan Huang, Jiqun Wang, Hongbo Men, Yi Tan, Qian Lin, Evelyne Gozal, Yang Zheng, Lu Cai

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Zinc flux in skin: Identity and function of metallothionein 1-positive cells in skin homeostasis.JID innovations : skin science from molecules to population health · 2026
    Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. 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

8 authors at 2 institutions in 2 countries.

Shan HuangDepartment of Pediatrics, Pediatric Research Institute, University of Louisville School of Medicine, Louisville, KY, USA.
Jiqun WangDepartment of Pediatrics, Pediatric Research Institute, University of Louisville School of Medicine, Louisville, KY, USA.
Hongbo MenDepartment of Pediatrics, Pediatric Research Institute, University of Louisville School of Medicine, Louisville, KY, USA.
Yi TanDepartment of Pediatrics, Pediatric Research Institute, University of Louisville School of Medicine, Louisville, KY, USA.
Qian LinDepartment of Pediatrics, Pediatric Research Institute, University of Louisville School of Medicine, Louisville, KY, USA.
Evelyne GozalDepartment of Pediatrics, Pediatric Research Institute, University of Louisville School of Medicine, Louisville, KY, USA.
Yang ZhengDepartment of Cardiovascular Disease, The First Hospital of Jilin University, Changchun, China.
Lu CaiDepartment of Pediatrics, Pediatric Research Institute, University of Louisville School of Medicine, Louisville, KY, USA.ORCID 0000-0003-3048-1135
University of Louisville · USJilin University · CN

Funding

University of Louisville Center for Integrative Environmental Health SciencesP30ES030283 · NIEHS · UNIVERSITY OF LOUISVILLE · PI Amanda Jo LeBlanc · 2020 to 2026
$10.0M
NIEHS NIH HHS P30 ES030283
6 · The paper itself

Abstract

To efficiently prevent diabetic cardiomyopathy (DCM), we have explored and confirmed that metallothionein (MT) prevents DCM by attenuating oxidative stress, and increasing expression of proteins associated with glucose metabolism. To determine whether Akt2 expression is critical to MT prevention of DCM, mice with either global Akt2 gene deletion (Akt2-KO), or cardiomyocyte-specific overexpressing MT gene (MT-TG) or both combined (MT-TG/Akt2-KO) were used. Akt2-KO mice exhibited symptoms of DCM (cardiac remodelling and dysfunction), and reduced expression of glycogen and glucose metabolism-related proteins, despite an increase in total Akt (t-Akt) phosphorylation. Cardiac MT overexpression in MT-TG/Akt2-KO mice prevented DCM and restored glucose metabolism-related proteins expression and baseline t-Akt phosphorylation. Furthermore, phosphorylation of ERK1/2 increased in the heart of MT-TG/Akt2-KO mice, compared with Akt2-KO mice. As ERK1/2 has been implicated in the regulation of glucose transport and metabolism this increase could potentially underlie MT protective effect in MT-TG/Akt2-KO mice. Therefore, these results show that although our previous work has shown that MT preserving Akt2 activity is sufficient to prevent DCM, in the absence of Akt2 MT may stimulate alternative or downstream pathways protecting from DCM in a type 2 model of diabetes, and that this protection may be associated with the ERK activation pathway.

Indexed as

AnimalsDiabetic CardiomyopathiesFemaleGlucoseHumansMaleMetallothioneinMiceMice, Inbred C57BLMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3MyocardiumProto-Oncogene Proteins c-aktTransgenesUp-RegulationAkt2 protein, mouseGlucoseMetallothioneinMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Proto-Oncogene Proteins c-aktAkt2 knock outdiabetesglucose metabolisminsulin resistancemetallothionein

Identifiers

PMID34053181
PMCPMC8278119
OpenAlexW3165018942

What Socratic 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 Socratic graph.