Evidence map›Paper›PMID 9410916›Full record

ArticleThe Journal of clinical investigation1997

Myosin heavy chain gene expression in human heart failure.

K Nakao, W Minobe, R Roden, M R Bristow, L A Leinwand

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 177 papers.

0numbers the graph read from it
0cells of the map it votes in
177citing papers in PubMed
12.6field-weighted citation impact, top 1% 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

177 citing papers in PubMed, 416 citations in OpenAlex.

  1. Trial
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  15. Cardiac wasting in patients with cancer.Basic research in cardiology · 2025
    Review
  16. Article
  17. Article
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  19. Article
  20. Review

117 more citing papers are in PubMed but not listed here.

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 1 country.

K NakaoDepartment of Molecular, Cellular and Developmental Biology, University of Colorado, Boulder 80309-0347, USA.
W Minobe
R Roden
M R Bristow
L A Leinwand
University of Colorado Health · USUniversity of Colorado Boulder · US

Funding

Genetic-Adrenergic Interactions in Myocardial FailureR01HL048013 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI BRISTOW, MICHAEL R. · 1993 to 2007
$4.5M
NHLBI NIH HHS 5R37 HL-50530-04NHLBI NIH HHS HL-48013
6 · The paper itself

Abstract

Two isoforms of myosin heavy chain (MyHC), alpha and beta, exist in the mammalian ventricular myocardium, and their relative expression is correlated with the contractile velocity of cardiac muscle. Several pathologic stimuli can cause a shift in the MyHC composition of the rodent ventricle from alpha- to beta-MyHC. Given the potential physiological consequences of cardiac MyHC isoform shifts, we determined MyHC gene expression in human heart failure where cardiac contractility is impaired significantly. In this study, we quantitated the relative amounts of alpha- and beta-MyHC mRNA in the left ventricular free walls (LVs) of 14 heart donor candidates with no history of cardiovascular disease or structural cardiovascular abnormalities. This group consisted of seven patients with nonfailing (NF) hearts and seven patients with hearts that exhibited donor heart dysfunction (DHD). These were compared with 19 patients undergoing cardiac transplantation for chronic end-stage heart failure (F). The relative amounts of alpha-MyHC mRNA to total (i.e., alpha + beta) MyHC mRNA in the NF- and DHD-LVs were surprisingly high compared with previous reports (33.3+/-18.9 and 35.4+/-16.5%, respectively), and were significantly higher than those in the F-LVs, regardless of the cause of heart failure (2.2+/-3.5%, P < 0.0001). There was no significant difference in the ratios in NF- and DHD-LVs. Our results demonstrate that a considerable amount of alpha-MyHC mRNA is expressed in the normal heart, and is decreased significantly in chronic end-stage heart failure. If protein and enzymatic activity correlate with mRNA expression, this molecular alteration may be sufficient to explain systolic dysfunction in F-LVs, and therapeutics oriented towards increasing alpha-MyHC gene expression may be feasible.

Indexed as

AdultBase SequenceFemaleGene ExpressionHeart FailureHeart VentriclesHumansMaleMiddle AgedMolecular Sequence DataMyosin Heavy ChainsMyosinsRNA, MessengerTissue DonorsMyosin Heavy ChainsMyosinsRNA, Messenger

Identifiers

PMID9410916
PMCPMC508434
OpenAlexW2014942570

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.