Evidence map›Paper›PMID 22155005›Full record

ArticleJournal of molecular and cellular cardiology2012

Enhanced desumoylation in murine hearts by overexpressed SENP2 leads to congenital heart defects and cardiac dysfunction.

Eun Young Kim, Li Chen, Yanlin Ma, Wei Yu, Jiang Chang, Ivan P Moskowitz, Jun Wang

Open access · greenAbstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

  1. Pooled it
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  18. The role of SUMOylation during development.Biochemical Society transactions · 2020
    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

7 authors at 4 institutions in 1 country.

Eun Young KimProgram in Genes and Development, The University of Texas Health Science Center at Houston, USA.
Li Chen
Yanlin Ma
Wei Yu
Jiang Chang
Ivan P Moskowitz
Jun Wang
St. Luke's Episcopal Hospital · USTexas A&M Health Science Center · USUniversity of Chicago · USUniversity of Houston · US

Funding

Genetic and Molecular Analysis of Mutants with Congenital Heart DefectsR01HL092153 · NHLBI · UNIVERSITY OF CHICAGO · PI MOSKOWITZ, IVAN PAUL · 2009 to 2017
$4.5M
Fibrogenic Role of ROCK delta1 and Mechanism in Cardiac RemodelingR01HL102314 · NHLBI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI CHANG, JIANG · 2010 to 2014
$1.8M
New Cardiovascular Research Scientist for Molecular and Cellular Biology CoreP30HL101336 · NHLBI · TEXAS HEART INSTITUTE · PI WILLERSON, JAMES T. · 2009 to 2010
$1.1M
Mechanism of SRF-N-mediated Cardiac SuppressionK02HL098956 · NHLBI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI CHANG, JIANG · 2010 to 2014
$471k
Mechanistic Study of Cleaved Serum Response Factor in Cardiac HypertrophyR21HL094844 · NHLBI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI CHANG, JIANG · 2010 to 2011
$403k
NHLBI NIH HHS 5R01HL102314-02NHLBI NIH HHS K02 HL098956NHLBI NIH HHS P30 HL101336NHLBI NIH HHS R01 HL092153NHLBI NIH HHS R01 HL102314NHLBI NIH HHS R21 HL094844
6 · The paper itself

Abstract

Sumoylation is a posttranslational modification implicated in a variety of cellular activities, and its role in a number of human pathogeneses such as cleft lip/palate has been well documented. However, the importance of the SUMO conjugation pathway in cardiac development and functional disorders is newly emerging. We previously reported that knockout of SUMO-1 in mice led to congenital heart diseases (CHDs). To further investigate the effects of imbalanced SUMO conjugation on heart development and function and its underlying mechanisms, we generated transgenic (Tg) mice with cardiac-specific expression of SENP2, a SUMO-specific protease that deconjugates sumoylated proteins, to evaluate the impact of desumoylation on heart development and function. Overexpression of SENP2 resulted in premature death of mice with CHDs-atrial septal defects (ASDs) and/or ventricular septal defects (VSDs). Immunobiochemistry revealed diminished cardiomyocyte proliferation in SENP2-Tg mouse hearts compared with that in wild type (WT) hearts. Surviving SENP2-Tg mice showed growth retardation, and developed cardiomyopathy with impaired cardiac function with aging. Cardiac-specific overexpression of the SUMO-1 transgene reduced the incidence of cardiac structural phenotypes in the sumoylation defective mice. Moreover, cardiac overexpression of SENP2 in the mice with Nkx2.5 haploinsufficiency promoted embryonic lethality and severity of CHDs, indicating the functional interaction between SENP2 and Nkx2.5 in vivo. Our findings indicate the indispensability of a balanced SUMO pathway for proper cardiac development and function. This article is part of a Special Issue entitled 'Post-translational Modification SI'.

Indexed as

SumoylationAnimalsCell LineCell ProliferationCysteine EndopeptidasesFemaleGene ExpressionGene Expression Regulation, DevelopmentalGenetic VectorsHeartHeart Defects, CongenitalHomeobox Protein Nkx-2.5Homeodomain ProteinsHumansMiceMice, Inbred C57BLCysteine EndopeptidasesHomeobox Protein Nkx-2.5Homeodomain ProteinsNkx2-5 protein, mouseSENP2 protein, humanSUMO-1 ProteinTranscription Factors

Identifiers

PMID22155005
PMCPMC3294171
OpenAlexW1981573620

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.