Evidence map›Paper›PMID 18466959›Full record

ReviewProgress in biophysics and molecular biology

The slow force response to stretch in atrial and ventricular myocardium from human heart: functional relevance and subcellular mechanisms.

Jens Kockskämper, Dirk von Lewinski, Mounir Khafaga, Andreas Elgner, Michael Grimm, Thomas Eschenhagen, Philip A Gottlieb, Frederick Sachs, Burkert Pieske

Open access · greenAbstract readReview
In one paragraph

Review in Progress in biophysics and molecular biology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 72 citations in OpenAlex.

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  19. Synergy between Piezo1 and Piezo2 channels confers high-strain mechanosensitivity to articular cartilage.Proceedings of the National Academy of Sciences of the United States of America · 2014
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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

9 authors at 4 institutions in 3 countries.

Jens KockskämperDepartment of Cardiology, Medical University of Graz, Auenbruggerplatz 15, Graz, Austria.
Dirk von Lewinski
Mounir Khafaga
Andreas Elgner
Michael Grimm
Thomas Eschenhagen
Philip A Gottlieb
Frederick Sachs
Burkert Pieske
Medical University of Graz · ATUniversität Hamburg · DEUniversity at Buffalo, State University of New York · USUniversitätsmedizin Göttingen · DE

Funding

Mechanosensitive ion channels and cortical mechanicsR01HL054887 · NHLBI · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI SACHS, FREDERICK · 1995 to 2016
$9.6M
NHLBI NIH HHS R01 HL054887
6 · The paper itself

Abstract

Mechanical load is an important regulator of cardiac force. Stretching human atrial and ventricular trabeculae elicited a biphasic force increase: an immediate increase (Frank-Starling mechanism) followed by a further slow increase (slow force response, SFR). In ventricle, the SFR was unaffected by AT- and ET-receptor antagonism, by inhibition of protein-kinase-C, PI-3-kinase, and NO-synthase, but attenuated by inhibition of Na+/H+- (NHE) and Na+/Ca2+ exchange (NCX). In atrium, however, neither NHE- nor NCX-inhibition affected the SFR. Stretch elicited a large NHE-dependent [Na+]i increase in ventricle but only a small, NHE-independent [Na+]i increase in atrium. Stretch-activated non-selective cation channels contributed to basal force development in atrium but not ventricle and were not involved in the SFR in either tissue. Interestingly, inhibition of AT receptors or pre-application of angiotensin II or endothelin-1 reduced the atrial SFR. Furthermore, stretch increased phosphorylation of atrial myosin light chain 2 (MLC2) and inhibition of myosin light chain kinase (MLCK) attenuated the SFR in atrium and ventricle. Thus, in human heart both atrial and ventricular myocardium exhibit a stretch-dependent SFR that might serve to adjust cardiac output to increased workload. In ventricle, there is a robust NHE-dependent (but angiotensin II- and endothelin-1-independent) [Na+]i increase that is translated into a [Ca2+]i and force increase via NCX. In atrium, on the other hand, there is an angiotensin II- and endothelin-dependent (but NHE- and NCX-independent) force increase. Increased myofilament Ca2+ sensitivity through MLCK-induced phosphorylation of MLC2 is a novel mechanism contributing to the SFR in both atrium and ventricle.

Indexed as

Angiotensin IICardiac MyosinsEndothelin-1HeartHeart AtriaHumansMyocardial ContractionMyocardiumMyosin Light ChainsNitric Oxide SynthaseProtein Kinase CSarcoplasmic ReticulumSodium-Calcium ExchangerSodium-Hydrogen ExchangersStress, MechanicalVentricular FunctionAngiotensin IICardiac MyosinsEndothelin-1myosin light chain 2Myosin Light ChainsNitric Oxide SynthaseProtein Kinase CSodium-Calcium ExchangerSodium-Hydrogen Exchangers

Identifiers

PMID18466959
PMCPMC2496926
OpenAlexW2076414120

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.