Evidence map›Paper›PMID 25125179›Full record

ReviewAnatomical record (Hoboken, N.J. : 2007)2014

Cell biology of sarcomeric protein engineering: disease modeling and therapeutic potential.

Brian R Thompson, Joseph M Metzger

Open access · greenAbstract readReview
In one paragraph

Review in Anatomical record (Hoboken, N.J. : 2007), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 26% 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

11 citing papers in PubMed, 21 citations in OpenAlex.

  1. Missense variants in the myosin binding domains ofbioRxiv : the preprint server for biology · 2025
    Article
  2. A transcriptional enhancer regulates cardiac maturation.Nature cardiovascular research · 2024
    Article
  3. Article
  4. Glycation in the cardiomyocyte.Vitamins and hormones · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Biology of the cardiac myocyte in heart disease.Molecular biology of the cell · 2016
    Review
  9. Review
  10. Article
  11. Recent advances in muscle research.Anatomical record (Hoboken, N.J. : 2007) · 2014
    Article
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

2 authors at 1 institution in 1 country.

Brian R ThompsonDepartment of Integrative Biology and Physiology, University of Minnesota Medical School, Minneapolis, Minnesota.
Joseph M Metzger
University of Minnesota Medical Center · US

Funding

TRAINING PROGRAM IN MUSCLE RESEARCHT32AR007612 · NIAMS · UNIVERSITY OF MINNESOTA TWIN CITIES · PI JAMES M ERVASTI, DAWN A LOWE · 2001 to 2026
$11.3M
Troponin and Heart Function in Heath and DiseaseR01HL059301 · NHLBI · UNIVERSITY OF MINNESOTA · PI METZGER, JOSEPH MARK · 1998 to 2014
$5.1M
Dystrophin Function in Aging HeartR01AG034107 · NIA · UNIVERSITY OF MINNESOTA · PI METZGER, JOSEPH MARK · 2010 to 2014
$1.7M
NHLBI NIH HHS 5R01 HL059301NHLBI NIH HHS R01 HL059301NIAMS NIH HHS 5 T32 AR 7612-9NIA NIH HHS 5R01 AG034107
6 · The paper itself

Abstract

The cardiac sarcomere is the functional unit for myocyte contraction. Ordered arrays of sarcomeric proteins, held in stoichiometric balance with each other, respond to calcium to coordinate contraction and relaxation of the heart. Altered sarcomeric structure-function underlies the primary basis of disease in multiple acquired and inherited heart disease states. Hypertrophic and restrictive cardiomyopathies are caused by inherited mutations in sarcomeric genes and result in altered contractility. Ischemia-mediated acidosis directly alters sarcomere function resulting in decreased contractility. In this review, we highlight the use of acute genetic engineering of adult cardiac myocytes through stoichiometric replacement of sarcomeric proteins in these disease states with particular focus on cardiac troponin I. Stoichiometric replacement of disease causing mutations has been instrumental in defining the molecular mechanisms of hypertrophic and restrictive cardiomyopathy in a cellular context. In addition, taking advantage of stoichiometric replacement through gene therapy is discussed, highlighting the ischemia-resistant histidine-button, A164H cTnI. Stoichiometric replacement of sarcomeric proteins offers a potential gene therapy avenue to replace mutant proteins, alter sarcomeric responses to pathophysiologic insults, or neutralize altered sarcomeric function in disease.

Indexed as

MutationProtein EngineeringAnimalsGenetic Predisposition to DiseaseGenetic TherapyHeart DiseasesHumansMuscle ProteinsMyocardiumPhenotypeSarcomeresMuscle Proteinsacute genetic engineeringadult cardiac myocytescalcium sensitivitymolecular dynamicsmyofilament, troponinsarcomere

Identifiers

PMID25125179
PMCPMC4133785
OpenAlexW1484389140

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.