Evidence map›Paper›PMID 22142594›Full record

ArticleJournal of molecular and cellular cardiology2012

Automated image analysis identifies signaling pathways regulating distinct signatures of cardiac myocyte hypertrophy.

Gregory T Bass, Karen A Ryall, Ashwin Katikapalli, Brooks E Taylor, Stephen T Dang, Scott T Acton, Jeffrey J Saucerman

Open access · greenAbstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

30 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Endothelial Nuclear and Cytoskeletal Responses to Mechanical Stresses.Advances in experimental medicine and biology · 2026
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  3. Article
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  5. Logic-based machine learning predicts how escitalopram attenuates cardiomyocyte hypertrophy.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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  18. The NCirculation · 2019
    Article
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  20. Review
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

7 authors at 1 institution in 1 country.

Gregory T BassDepartment of Biomedical Engineering, University of Virginia, Charlottesville, VA 22908-0759, USA.
Karen A Ryall
Ashwin Katikapalli
Brooks E Taylor
Stephen T Dang
Scott T Acton
Jeffrey J Saucerman
University of Virginia · US

Funding

Quantitative analysis of cAMP compartmentation in heartR01HL094476 · NHLBI · UNIVERSITY OF VIRGINIA · PI SAUCERMAN, JEFFREY J. · 2009 to 2013
$1.8M
NHLBI NIH HHS HL094476NHLBI NIH HHS R01 HL094476
6 · The paper itself

Abstract

Cardiac hypertrophy is controlled by a complex signal transduction and gene regulatory network, containing multiple layers of crosstalk and feedback. While numerous individual components of this network have been identified, understanding how these elements are coordinated to regulate heart growth remains a challenge. Past approaches to measure cardiac myocyte hypertrophy have been manual and often qualitative, hindering the ability to systematically characterize the network's higher-order control structure and identify therapeutic targets. Here, we develop and validate an automated image analysis approach for objectively quantifying multiple hypertrophic phenotypes from immunofluorescence images. This approach incorporates cardiac myocyte-specific optimizations and provides quantitative measures of myocyte size, elongation, circularity, sarcomeric organization, and cell-cell contact. As a proof-of-concept, we examined the hypertrophic response to α-adrenergic, β-adrenergic, tumor necrosis factor (TNFα), insulin-like growth factor-1 (IGF-1), and fetal bovine serum pathways. While all five hypertrophic pathways increased myocyte size, other hypertrophic metrics were differentially regulated, forming a distinct phenotype signature for each pathway. Sarcomeric organization was uniquely enhanced by α-adrenergic signaling. TNFα and α-adrenergic pathways markedly decreased cell circularity due to increased myocyte protrusion. Surprisingly, adrenergic and IGF-1 pathways differentially regulated myocyte-myocyte contact, potentially forming a feed-forward loop that regulates hypertrophy. Automated image analysis unlocks a range of new quantitative phenotypic data, aiding dissection of the complex hypertrophic signaling network and enabling myocyte-based high-content drug screening.

Indexed as

Image Processing, Computer-AssistedSignal TransductionAdrenergic alpha-AgonistsAdrenergic beta-AgonistsAnimalsCardiomegalyCell AdhesionCell EnlargementCells, CulturedCell ShapeCell SizeInsulin-Like Growth Factor IIsoproterenolMyocytes, CardiacPhenotypePhenylephrineAdrenergic alpha-AgonistsAdrenergic beta-AgonistsInsulin-Like Growth Factor IIsoproterenolPhenylephrineTumor Necrosis Factor-alpha

Identifiers

PMID22142594
PMCPMC3299901
OpenAlexW2074477987

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.