Evidence map›Paper›PMID 30707448›Full record

ArticleThe Journal of physiology2019

Cardiomyocyte substructure reverts to an immature phenotype during heart failure.

D B Lipsett, M Frisk, J M Aronsen, E S Nordén, O R Buonarati, A Cataliotti, J W Hell, I Sjaastad, G Christensen, W E Louch

Open access · hybridAbstract read
In one paragraph

Article in The Journal of physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 4% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

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  9. Nanoscale organization of cardiac calcium channels is dependent on thyroid hormone status.American journal of physiology. Heart and circulatory physiology · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 2 countries.

D B LipsettInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway.
M FriskInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway.
J M AronsenInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway.
E S NordénInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway.
O R BuonaratiDepartment of Pharmacology, University of California Davis, Davis, CA, USA.ORCID 0000-0001-6530-6797
A CataliottiInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway.
J W HellDepartment of Pharmacology, University of California Davis, Davis, CA, USA.ORCID 0000-0001-7960-7531
I SjaastadInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway.
G ChristensenInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway.
W E LouchInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway.ORCID 0000-0002-0511-6112
Oslo University Hospital · NOUniversity of California, Davis · US

Funding

Role of a-actinin in Cav1.2 FunctionR01AG055357 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI JOHANNES W HELL · 2016 to 2026
$4.0M
NIA NIH HHS R01 AG055357
6 · The paper itself

Abstract

key pointsAs reactivation of the fetal gene program has been implicated in pathological remodelling during heart failure (HF), we examined whether cardiomyocyte subcellular structure and function revert to an immature phenotype during this disease. Surface and internal membrane structures appeared gradually during development, and returned to a juvenile state during HF. Similarly, dyadic junctions between the cell membrane and sarcoplasmic reticulum were progressively 'packed' with L-type Ca ABSTRACT: Reactivation of the fetal gene programme has been implicated as a driver of pathological cardiac remodelling. Here we examined whether pathological remodelling of cardiomyocyte substructure and function during heart failure (HF) reflects a reversion to an immature phenotype. Using scanning electron microscopy, we observed that Z-grooves and t-tubule openings at the cell surface appeared gradually during cardiac development, and disappeared during HF. Confocal and super-resolution imaging within the cell interior revealed similar structural parallels; disorganization of t-tubules in failing cells was strikingly reminiscent of the late stages of postnatal development, with fewer transverse elements and a high proportion of longitudinal tubules. Ryanodine receptors (RyRs) were observed to be laid down in advance of developing t-tubules and similarly 'orphaned' in HF, although RyR distribution along Z-lines was relatively sparse. Indeed, nanoscale imaging revealed coordinated packing of L-type Ca

Indexed as

Heart FailureAnimalsCalciumFemaleMaleMicroscopy, ConfocalMyocardial InfarctionMyocytes, CardiacPregnancyRatsRats, WistarRyanodine Receptor Calcium Release ChannelCalciumRyanodine Receptor Calcium Release Channelcalcium homeostasisdevelopmentdyadheart failuret-tubule

Identifiers

PMID30707448
PMCPMC6441900
OpenAlexW2920793939

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.