Evidence map›Paper›PMID 24064296›Full record

ArticleCardiovascular research2014

Loss of β2-spectrin prevents cardiomyocyte differentiation and heart development.

Jeong A Lim, Hye Jung Baek, Moon Sun Jang, Eun Kyoung Choi, Yong Min Lee, Sang Jin Lee, Sung Chul Lim, Joo Young Kim, Tae Hyun Kim, Hye Sun Kim and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Cardiovascular research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 31% 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

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

  1. Pooled it
  2. Article
  3. Postsynaptic β1 spectrin maintains NaThe Journal of physiology · 2024
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  17. Dysfunction of the β2-spectrin-based pathway in human heart failure.American journal of physiology. Heart and circulatory physiology · 2016
    Article
  18. Article
  19. Article
  20. Endothelial βII Spectrin Deletion Exacerbates Inflammation and Impairs Tissue Regeneration in Ischemic-Diabetic Skin Wound Healing.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society
    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

12 authors at 3 institutions in 2 countries.

Jeong A LimRadiation Medicine Branch, National Cancer Center, 323 Ilsan-ro, Ilsandong-gu, Goyang-si, Gyeonggi-do, Goyang 410-769, Korea.
Hye Jung Baek
Moon Sun Jang
Eun Kyoung Choi
Yong Min Lee
Sang Jin Lee
Sung Chul Lim
Joo Young Kim
Tae Hyun Kim
Hye Sun Kim
Lopa Mishra
Sang Soo Kim
National Cancer Center · KRAjou University · KRThe University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Targeting CDK4 in TGS-B Inactivated Gastrointestinal CancersP01CA130821 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI MISHRA, LOPA · 2008 to 2013
$6.9M
NCI NIH HHS P01 CA130821NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

aimsβ2-Spectrin is an actin-binding protein that plays an important role in membrane integrity and the transforming growth factor (TGF)-β signalling pathway as an adaptor for Smads. Loss of β2-spectrin in mice (Spnb2(-/-)) results in embryonic lethality with gastrointestinal, liver, neural, and heart abnormalities that are similar to those in Smad2(+/-)Smad3(+/-) mice. However, to date, the role of β2-spectrin in embryogenesis, particularly in heart development, has been poorly delineated. Here, we demonstrated that β2-spectrin is required for the survival and differentiation of cardiomyocytes, and its loss resulted in defects in heart development with failure of ventricular wall thickening. METHODS AND

resultsDisruption of β2-spectrin in primary muscle cells not only inhibited TGF-β/Smad signalling, but also reduced the expression of the cardiomyocyte differentiation markers Nkx2.5, dystrophin, and α-smooth muscle actin (α-SMA). Furthermore, cytoskeletal networks of dystrophin, F-actin, and α-SMA in cardiomyocytes were disorganized upon loss of β2-spectrin. In addition, deletion of β2-spectrin in mice (Spnb2(tm1a/tm1a)) prevented proper development of the heart in association with disintegration of dystrophin structure and markedly reduced survival.

conclusionThese data suggest that β2-spectrin deficiency leads to inactivation of TGF-β/Smad signalling and contributes to dysregulation of the cell cycle, proliferation, differentiation, and the cytoskeletal network, and it leads to defective heart development. Our data demonstrate that β2-spectrin is required for proper development of the heart and that disruption of β2-spectrin is a potential underlying cause of congenital heart defects.

Indexed as

Cell DifferentiationAnimalsApoptosisCarrier ProteinsCell ProliferationCells, CulturedCytoskeletal ProteinsDystrophinFemaleHeartHeart Defects, CongenitalMaleMice, Inbred C57BLMicrofilament ProteinsMyocytes, CardiacMyofibrilsCarrier ProteinsCytoskeletal ProteinsDystrophinMicrofilament ProteinsSmad ProteinsSpectrinTransforming Growth Factor betaCardiogenesisCytoskeletonTGF-ββ2-Spectrin

Identifiers

PMID24064296
PMCPMC4229887
OpenAlexW2106618944

What OpenQuestion holds

Textmetadata
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.