Evidence map›Paper›PMID 27184165›Full record

ArticleArchives of biochemistry and biophysics2016

Diastolic dysfunction and cardiac troponin I decrease in aging hearts.

B Pan, Z W Xu, Y Xu, L J Liu, J Zhu, X Wang, C Nan, Z Zhang, W Shen, X P Huang and 1 more

Abstract read
In one paragraph

Article in Archives of biochemistry and biophysics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

14 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
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  9. Mechanisms and implications of sex differences in cardiac aging.The journal of cardiovascular aging · 2022
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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

11 authors at 1 institution in 1 country.

B PanHeart Centre, Children's Hospital of Chongqing Medical University, Chongqing, PR China; Key Laboratory of Developmental Disease in Childhood (Chongqing Medical University), Ministry of Education, Chongqing, PR China; Key Laboratory of Pediatrics in Chongqing, PR China; Chongqing International Science and Technology Cooperation Center for Child Development and Disorders, PR China.
Z W XuHeart Centre, Children's Hospital of Chongqing Medical University, Chongqing, PR China; Key Laboratory of Developmental Disease in Childhood (Chongqing Medical University), Ministry of Education, Chongqing, PR China; Key Laboratory of Pediatrics in Chongqing, PR China; Chongqing International Science and Technology Cooperation Center for Child Development and Disorders, PR China.
Y XuHeart Centre, Children's Hospital of Chongqing Medical University, Chongqing, PR China; Key Laboratory of Developmental Disease in Childhood (Chongqing Medical University), Ministry of Education, Chongqing, PR China; Key Laboratory of Pediatrics in Chongqing, PR China; Chongqing International Science and Technology Cooperation Center for Child Development and Disorders, PR China.
L J LiuKey Laboratory of Developmental Disease in Childhood (Chongqing Medical University), Ministry of Education, Chongqing, PR China; Key Laboratory of Pediatrics in Chongqing, PR China; Chongqing International Science and Technology Cooperation Center for Child Development and Disorders, PR China.
J ZhuKey Laboratory of Developmental Disease in Childhood (Chongqing Medical University), Ministry of Education, Chongqing, PR China; Key Laboratory of Pediatrics in Chongqing, PR China; Chongqing International Science and Technology Cooperation Center for Child Development and Disorders, PR China.
X WangDepartment of Biomedical Science, Charlie E. Schmidt College of Medicine, Florida Atlantic University, Boca Raton, FL, USA.
C NanDepartment of Biomedical Science, Charlie E. Schmidt College of Medicine, Florida Atlantic University, Boca Raton, FL, USA.
Z ZhangDepartment of Biomedical Science, Charlie E. Schmidt College of Medicine, Florida Atlantic University, Boca Raton, FL, USA.
W ShenDepartment of Biomedical Science, Charlie E. Schmidt College of Medicine, Florida Atlantic University, Boca Raton, FL, USA.
X P HuangDepartment of Biomedical Science, Charlie E. Schmidt College of Medicine, Florida Atlantic University, Boca Raton, FL, USA. Electronic address: xhuang@health.fau.edu.
J TianHeart Centre, Children's Hospital of Chongqing Medical University, Chongqing, PR China. Electronic address: jietian@cqmu.edu.cn.
Florida Atlantic University · US

Funding

Restrictive Cardiomyopathy Caused by Cardiac Troponin MutationsR15HL112130 · NHLBI · FLORIDA ATLANTIC UNIVERSITY · PI HUANG, XUPEI · 2012 to 2012
$434k
NHLBI NIH HHS R15 HL112130
6 · The paper itself

Abstract

Cardiac tropnoin I (cTnI) plays a critical role in the regulation of diastolic function, and its low expression may result in cardiac diastolic dysfunction, which is the most common form of cardiovascular disorders in older adults. In this study, cTnI expression levels were determined in mice at various ages and cardiac function was measured and compared between young adult mice (3 and 10 months) and older mice (18 months). The data indicated that the cTnI levels reached a peak high in young adult hearts (3 months), but decreased in older hearts (18 months). Furthermore, the older hearts showed a significant diastolic dysfunction observed by P-V loop and echocardiography measurements. To further define the mechanism underlying the cTnI decrease in aging hearts, we tested DNA methylation and histone acetylation modifications of cTnI gene. We found that acetylation of histone near the promoter region of cTnI gene played an important role in regulation of cTnI expression in the heart at different ages. Our study indicates that epigenetic modification caused cTnI expression decrease is one of the possible causes that result in a reduced cTnI level and diastolic dysfunction in the older hearts.

Indexed as

AgingDiastoleAnimalsCardiomyopathiesChromatin ImmunoprecipitationEchocardiographyEpigenesis, GeneticHeartMiceMice, Inbred C57BLMyocardiumMyocytes, CardiacPromoter Regions, GeneticTroponin ITroponin IDiastolic dysfunctionEpigeneticsGene expressionHistone acetylationTroponin

Identifiers

PMID27184165
PMCPMC5448708
OpenAlexW2358484352

What OpenQuestion holds

Textmetadata
LicenceTDM
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.