Evidence map›Paper›PMID 19649240›Full record

ArticleExperimental and clinical cardiology2002

A molecular mechanism improving the contractile state in human myocardial hypertrophy.

Oliver Ritter, Nico Bottez, Natalie Burkard, Hagen D Schulte, Ludwig Neyses

Open access · greenAbstract read
PubMed Full text at PMC
In one paragraph

Article in Experimental and clinical cardiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact, top 80% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

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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

5 authors at 2 institutions in 2 countries.

Oliver RitterDepartment of Medicine, University of Wuerzburg, Germany;
Nico Bottez
Natalie Burkard
Hagen D Schulte
Ludwig Neyses
University of Luxembourg · LUUniversity of Würzburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundVarious molecular mechanisms are operative in altering the sarcomeric function of the heart under increased hemodynamic workload. Expression of the atrial isoform (ALC-1) of the essential myosin light chain, a shift from alpha-myosin heavy chain (MHC) to beta-MHC, increased phosphorylation of the regulatory myosin light chains and increased troponin I (TnI) phosphorylation have been reported to modulate cardiac contractility in rodents.

methodsTO ASSESS A POSSIBLE CONTRIBUTION OF THESE SARCOMERIC PROTEINS TO CARDIAC PERFORMANCE IN HUMAN MYOCARDIAL HYPERTROPHY, TWO DIFFERENT FORMS OF CARDIAC HYPERTROPHY WERE INVESTIGATED: 19 patients with hypertropic obstructive cardiomyopathy (HOCM) and 13 patients with aortic stenosis (AS) with marked left ventricular hypertrophy and normal systolic function.

resultsThere was no change in MHC gene expression, regulatory myosin light chain or TnI phosphorylation status in normal heart (NH), HOCM and AS patients. However, patients with hypertrophied myocardium expressed ALC-1 that was not detectable in NH. ALC-1 protein expression correlated positively with the left ventricular ejection fraction. In patients with hypertrophied myocardium, there was a mean ALC-1 protein expression of 12.7+/-3% (range 3.6% to 32%).

conclusionIn humans, ALC-1 expression is in vivo a powerful molecular mechanism of the sarcomere to maintain or improve myocardial contractility under increased hemodynamic demands.

Indexed as

Myocardial hypertrophyMyosin light chains

Identifiers

PMID19649240
PMCPMC2719172
OpenAlexW2126833120

What OpenQuestion holds

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Registered trials

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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.