Evidence map›Paper›PMID 25354087›Full record

ArticlePloS one2014

Myeloid mineralocorticoid receptor deficiency inhibits aortic constriction-induced cardiac hypertrophy in mice.

Chao Li, Yu Yao Zhang, Ryan A Frieler, Xiao Jun Zheng, Wu Chang Zhang, Xue Nan Sun, Qing Zhen Yang, Shu Min Ma, Baozhuan Huang, Stefan Berger and 5 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

24 citing papers in PubMed, 50 citations in OpenAlex.

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  15. CCR2JACC. Basic to translational science · 2018
    Article
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  17. Role of mineralocorticoid receptor activation in cardiac diastolic dysfunction.Biochimica et biophysica acta. Molecular basis of disease · 2017
    Review
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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

15 authors at 7 institutions in 3 countries.

Chao LiKey Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Yu Yao ZhangKey Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Ryan A FrielerDepartment of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan, United States of America; Department of Pharmacology, University of Michigan Medical School, Ann Arbor, Michigan, United States of America.
Xiao Jun ZhengKey Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Wu Chang ZhangKey Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Xue Nan SunKey Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Qing Zhen YangKey Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Shu Min MaKey Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Baozhuan HuangDepartment of Nephrology, Xuhui Central Hospital, Shanghai, China.
Stefan BergerGerman Cancer Research Center (DKFZ), Division Molecular Biology of the Cell I, Heidelberg, Germany.
Wang WangMitochondria and Metabolism Center, Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, Washington, United States of America.
Yong WuDivision of Cancer Research and Training, Department of Internal Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, California, United States of America; David Geffen School of Medicine at University of California Los Angeles, Los Angeles, California, United States of America.
Ying YuKey Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Sheng Zhong DuanKey Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Richard M MortensenDepartment of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan, United States of America; Department of Pharmacology, University of Michigan Medical School, Ann Arbor, Michigan, United States of America; Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan, United States of America.
Chinese Academy of Sciences · CNShanghai Institutes for Biological Sciences · CNUniversity of Michigan–Ann Arbor · USHeidelberg University · DEShanghai Xuhui Central Hospital · CNUniversity of California, Los Angeles · USUniversity of Washington · US

Funding

Myeloid Reprogramming in Cardiac Protection by Aldosterone AntagonistsR01HL112610 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MORTENSEN, RICHARD M · 2014 to 2017
$1.6M
Metabolic responsive factors in cardiovascular diseaseR01HL083201 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MORTENSEN, RICHARD M · 2006 to 2009
$1.5M
Regulation of Macrophage Phenotypes during Neuroinflammation and StrokeF31NS077780 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FRIELER, RYAN ALLEN · 2012 to 2013
$66k
NHLBI NIH HHS R01 HL083201NHLBI NIH HHS R01HL083201NHLBI NIH HHS R01 HL112610NINDS NIH HHS F31 NS077780
6 · The paper itself

Abstract

Mineralocorticoid receptor (MR) blockade has been shown to suppress cardiac hypertrophy and remodeling in animal models of pressure overload (POL). This study aims to determine whether MR deficiency in myeloid cells modulates aortic constriction-induced cardiovascular injuries. Myeloid MR knockout (MMRKO) mice and littermate control mice were subjected to abdominal aortic constriction (AAC) or sham operation. We found that AAC-induced cardiac hypertrophy and fibrosis were significantly attenuated in MMRKO mice. Expression of genes important in generating reactive oxygen species was decreased in MMRKO mice, while that of manganese superoxide dismutase increased. Furthermore, expression of genes important in cardiac metabolism was increased in MMRKO hearts. Macrophage infiltration in the heart was inhibited and expression of inflammatory genes was decreased in MMRKO mice. In addition, aortic fibrosis and inflammation were attenuated in MMRKO mice. Taken together, our data indicated that MR deficiency in myeloid cells effectively attenuated aortic constriction-induced cardiac hypertrophy and fibrosis, as well as aortic fibrosis and inflammation.

Indexed as

AnimalsAorta, AbdominalConstriction, PathologicGene Expression RegulationHypertrophy, Left VentricularMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutReactive Oxygen SpeciesReceptors, MineralocorticoidNr3c2 protein, mouseReactive Oxygen SpeciesReceptors, Mineralocorticoid

Identifiers

PMID25354087
PMCPMC4212990
OpenAlexW2064658949

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.