Evidence map›Paper›PMID 25177426›Full record

ArticleOxidative medicine and cellular longevity2014

Deletion of metallothionein exacerbates intermittent hypoxia-induced oxidative and inflammatory injury in aorta.

Shanshan Zhou, Yonggang Wang, Yi Tan, Xiaohong Cai, Lu Cai, Jun Cai, Yang Zheng

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

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  17. CuFrontiers in neuroscience · 2018
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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 5 institutions in 2 countries.

Shanshan ZhouThe Center of Cardiovascular Diseases at the First Hospital of Jilin University, 71 Xinmin Street, Changchun 130021, China ; Kosair Children's Hospital Research Institute at the Department of Pediatrics, University of Louisville, 570 South Preston Street, Baxter I, Suite 321B, Louisville, KY 40202, USA.
Yonggang WangThe Center of Cardiovascular Diseases at the First Hospital of Jilin University, 71 Xinmin Street, Changchun 130021, China ; Kosair Children's Hospital Research Institute at the Department of Pediatrics, University of Louisville, 570 South Preston Street, Baxter I, Suite 321B, Louisville, KY 40202, USA.
Yi TanKosair Children's Hospital Research Institute at the Department of Pediatrics, University of Louisville, 570 South Preston Street, Baxter I, Suite 321B, Louisville, KY 40202, USA ; Chinese-American Research Institute for Diabetic Complication, Wenzhou Medical College, Wenzhou 325035, China.
Xiaohong CaiDepartment of Pediatrics, The Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325027, China.
Lu CaiKosair Children's Hospital Research Institute at the Department of Pediatrics, University of Louisville, 570 South Preston Street, Baxter I, Suite 321B, Louisville, KY 40202, USA ; Departments of Radiation Oncology and Pharmacology and Toxicology, University of Louisville, Louisville, KY 40202, USA.
Jun CaiKosair Children's Hospital Research Institute at the Department of Pediatrics, University of Louisville, 570 South Preston Street, Baxter I, Suite 321B, Louisville, KY 40202, USA.
Yang ZhengThe Center of Cardiovascular Diseases at the First Hospital of Jilin University, 71 Xinmin Street, Changchun 130021, China.
Kosair Children's Hospital · USFirst Hospital of Jilin University · CNJilin University · CNUniversity of Louisville · USWenzhou Medical University · CN

Funding

Molecular Determinants of Developmental DefectsP20GM103453 · NIGMS · UNIVERSITY OF LOUISVILLE · PI GREENE, ROBERT M · 2012 to 2012
$1.7M
NIGMS NIH HHS P20 GM103453
6 · The paper itself

Abstract

The present study was to explore the effect of metallothionein (MT) on intermittent hypoxia (IH) induced aortic pathogenic changes. Markers of oxidative damages, inflammation, and vascular remodeling were observed by immunohistochemical staining after 3 days and 1, 3, and 8 weeks after IH exposures. Endogenous MT was induced after 3 days of IH but was significantly decreased after 8 weeks of IH. Compared with the wild-type mice, MT knock-out mice exhibited earlier and more severe pathogenic changes of oxidative damages, inflammatory responses, and cellular apoptosis, as indicated by the significant accumulation of collagen, increased levels of connective tissue growth factor, transforming growth factor β1, tumor necrosis factor-alpha, vascular cell adhesion molecule 1,3-nitrotyrosine, and 4-hydroxy-2-nonenal in the aorta. These findings suggested that chronic IH may lead to aortic damages characterized by oxidative stress and inflammation, and MT may play a pivotal role in the above pathogenesis process.

Indexed as

HypoxiaOxidative StressAldehydesAnimalsAortaApoptosisConnective Tissue Growth FactorMetallothioneinMiceMice, KnockoutNADPH OxidasesNitric Oxide Synthase Type IIITime FactorsTumor Necrosis Factor-alphaTyrosine3-nitrotyrosine4-hydroxy-2-nonenalAldehydesCCN2 protein, mouseConnective Tissue Growth FactorMetallothioneinNADPH Oxidasesneutrophil cytosolic factor 1Nitric Oxide Synthase Type IIINos3 protein, mouseTumor Necrosis Factor-alphaTyrosine

Identifiers

PMID25177426
PMCPMC4142187
OpenAlexW2087321034

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.