Evidence map›Paper›PMID 22496245›Full record

ArticleAmerican journal of physiology. Cell physiology2012

Ablation of sarcolipin results in atrial remodeling.

Lai-Hua Xie, Mayilvahanan Shanmugam, Ji Yeon Park, Zhenghang Zhao, Hairuo Wen, Bin Tian, Muthu Periasamy, Gopal J Babu

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Altered contractility, CaAmerican journal of physiology. Heart and circulatory physiology · 2023
    Article
  4. Mouse models of spontaneous atrial fibrillation.Mammalian genome : official journal of the International Mammalian Genome Society · 2023
    Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Sarcolipin haploinsufficiency prevents dystrophic cardiomyopathy inAmerican journal of physiology. Heart and circulatory physiology · 2021
    Article
  10. SERCA2a: a key protein in the CaHeart failure reviews · 2020
    Review
  11. Primary Active CaCold Spring Harbor perspectives in biology · 2020
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

8 authors at 3 institutions in 1 country.

Lai-Hua XieDepartment of Cell Biology and Molecular Medicine, University of Medicine and Dentistry of New Jersey-New Jersey Medical School, Newark, 07103, USA.
Mayilvahanan Shanmugam
Ji Yeon Park
Zhenghang Zhao
Hairuo Wen
Bin Tian
Muthu Periasamy
Gopal J Babu
Rutgers, The State University of New Jersey · USRutgers New Jersey Medical SchoolThe Ohio State University · US

Funding

Alternative mRNA processing in cardiac hypertrophyR21HL098802 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI TIAN, BIN · 2010 to 2011
$429k
NHLBI NIH HHS HL 080551NHLBI NIH HHS HL097878
6 · The paper itself

Abstract

Sarcolipin (SLN) is a key regulator of sarco(endo)plasmic reticulum (SR) Ca(2+)-ATPase (SERCA), and its expression is altered in diseased atrial myocardium. To determine the precise role of SLN in atrial Ca(2+) homeostasis, we developed a SLN knockout (sln-/-) mouse model and demonstrated that ablation of SLN enhances atrial SERCA pump activity. The present study is designed to determine the long-term effects of enhanced SERCA activity on atrial remodeling in the sln-/- mice. Calcium transient measurements show an increase in atrial SR Ca(2+) load and twitch Ca(2+) transients. Patch-clamping experiments demonstrate activation of the forward mode of sodium/calcium exchanger, increased L-type Ca(2+) channel activity, and prolongation of action potential duration at 90% repolarization in the atrial myocytes of sln-/- mice. Spontaneous Ca(2+) waves, delayed afterdepolarization, and triggered activities are frequent in the atrial myocytes of sln-/- mice. Furthermore, loss of SLN in atria is associated with increased interstitial fibrosis and altered expression of genes encoding collagen and other extracellular matrix proteins. Our results also show that the sln-/- mice are susceptible to atrial arrhythmias upon aging. Together, these findings indicate that ablation of SLN results in increased SERCA activity and SR Ca(2+) load, which, in turn, could cause abnormal intracellular Ca(2+) handling and atrial remodeling.

Indexed as

Atrial FunctionCalcium SignalingAction PotentialsAgingAnimalsArrhythmias, CardiacCalcium Channels, L-TypeCollagenFibrosisGene Expression RegulationGenotypeHeart AtriaHomeostasisMiceMice, Inbred C57BLMice, KnockoutCalcium Channels, L-TypeCollagenMuscle ProteinsProteolipidssarcolipinSarcoplasmic Reticulum Calcium-Transporting ATPases

Identifiers

PMID22496245
PMCPMC3378074
OpenAlexW1983690275

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.