Evidence map›Paper›PMID 25858069›Full record

ReviewCirculation research2015

Mechanotransduction in cardiac hypertrophy and failure.

Robert C Lyon, Fabian Zanella, Jeffrey H Omens, Farah Sheikh

Open access · bronzeAbstract readReview
In one paragraph

Review in Circulation research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 208 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
208citing papers in PubMed, 2 pooled it
17.0field-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

208 citing papers in PubMed, 2 syntheses or guidelines pooled it, 327 citations in OpenAlex.

  1. Pooled it
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  5. A modelling study of right ventricular growth with valvular regurgitation.Biomechanics and modeling in mechanobiology · 2026
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148 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

4 authors at 1 institution in 1 country.

Robert C Lyon *Department of Medicine, University of California San Diego, 9500 Gilman Drive, La Jolla, CA, 92093, USA.
Fabian Zanella *Department of Medicine, University of California San Diego, 9500 Gilman Drive, La Jolla, CA, 92093, USA.
Jeffrey H OmensDepartment of Medicine, University of California San Diego, 9500 Gilman Drive, La Jolla, CA, 92093, USA.
Farah SheikhDepartment of Medicine, University of California San Diego, 9500 Gilman Drive, La Jolla, CA, 92093, USA.
La Jolla Bioengineering Institute · US

Funding

The Virtual Physiological Rat ProjectP50GM094503 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BEARD, DANIEL A · 2011 to 2015
$11.6M
Training In Cardiovascular Physiology & PharmacologyT32HL007444 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Ju Chen, Robert Scott Ross · 1985 to 2026
$11.1M
The molecular mechanisms underlying arrhythmogenic right ventricular dysplasia/cardiomyopathyR01HL095780 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SHEIKH, FARAH · 2009 to 2018
$3.9M
Multi-scale Systems Model of Murine Heart FailureR01HL105242 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BERS, DONALD M, MCCULLOCH, ANDREW D. · 2012 to 2016
$3.5M
Cardiomyocyte mechanotransduction through the integrin complexR01HL103566 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI OMENS, JEFFREY H., ROSS, ROBERT SCOTT · 2010 to 2014
$1.9M
ANALYSIS OF AX1 RECEPTOR SIGNAL TRANSDUCTIONF32HL009780 · NHLBI · UNIVERSITY OF WASHINGTON · PI MELARAGNO, MATTHEW G · 1997 to 1999
–
NHLBI NIH HHS F32 HL009780NHLBI NIH HHS HL09780NHLBI NIH HHS HL103566NHLBI NIH HHS HL105242NHLBI NIH HHS R01 HL095780NHLBI NIH HHS R01 HL103566NHLBI NIH HHS R01 HL105242NHLBI NIH HHS T32 HL007444NIGMS NIH HHS P50 GM094503
6 · The paper itself

Abstract

Cardiac muscle cells have an intrinsic ability to sense and respond to mechanical load through a process known as mechanotransduction. In the heart, this process involves the conversion of mechanical stimuli into biochemical events that induce changes in myocardial structure and function. Mechanotransduction and its downstream effects function initially as adaptive responses that serve as compensatory mechanisms during adaptation to the initial load. However, under prolonged and abnormal loading conditions, the remodeling processes can become maladaptive, leading to altered physiological function and the development of pathological cardiac hypertrophy and heart failure. Although the mechanisms underlying mechanotransduction are far from being fully elucidated, human and mouse genetic studies have highlighted various cytoskeletal and sarcolemmal structures in cardiac myocytes as the likely candidates for load transducers, based on their link to signaling molecules and architectural components important in disease pathogenesis. In this review, we summarize recent developments that have uncovered specific protein complexes linked to mechanotransduction and mechanotransmission within the sarcomere, the intercalated disc, and at the sarcolemma. The protein structures acting as mechanotransducers are the first step in the process that drives physiological and pathological cardiac hypertrophy and remodeling, as well as the transition to heart failure, and may provide better insights into mechanisms driving mechanotransduction-based diseases.

Indexed as

HemodynamicsMechanotransduction, CellularAdaptation, PhysiologicalAnimalsCardiomegalyHeart FailureHumansMultiprotein ComplexesMuscle ProteinsMyocytes, CardiacMultiprotein ComplexesMuscle Proteinscytoskeletonheartheart failureintercellular junctionsmechanotransduction, cellularmyocardiumsarcolemmasarcomeres

Identifiers

PMID25858069
PMCPMC4394185
OpenAlexW1977303730

What OpenQuestion holds

Textmetadata
LicenceTDM
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.