Evidence map›Paper›PMID 26776594›Full record

ReviewJournal of veterinary cardiology : the official journal of the European Society of Veterinary Cardiology2015

The genetic basis of hypertrophic cardiomyopathy in cats and humans.

Mark D Kittleson, Kathryn M Meurs, Samantha P Harris

Open access · greenAbstract readReview
In one paragraph

Review in Journal of veterinary cardiology : the official journal of the European Society of Veterinary Cardiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.1field-weighted citation impact, top 11% 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

41 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
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  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Genetic Basis of Hypertrophic Cardiomyopathy in Cats.Current issues in molecular biology · 2024
    Review
  13. Article
  14. The Role of Personalized Medicine in Companion Animal Cardiology.The Veterinary clinics of North America. Small animal practice · 2023
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 1 country.

Mark D KittlesonDepartment of Medicine and Epidemiology, University of California, Davis, Davis, CA 95616, USA. Electronic address: mdkittleson@ucdavis.edu.
Kathryn M MeursDepartment of Veterinary Clinical Sciences, North Carolina State University, Raleigh, NC 27607, USA.
Samantha P HarrisDepartment of Cellular and Molecular Medicine, University of Arizona, Tucson, AZ 85721, USA.
North Carolina State University · USUniversity of Arizona · USUniversity of California, Davis · US

Funding

Role of Myosin Binding Protein-C in the Regulation of Myocardial ContractionR01HL080367 · NHLBI · UNIVERSITY OF WASHINGTON · PI Samantha P Harris · 2005 to 2026
$7.5M
Molecular Mechanisms of Disease in a Novel Feline Model of Familial HypertrophicR21HL093603 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI HARRIS, SAMANTHA P · 2010 to 2011
$418k
NHLBI NIH HHS R01 HL080367NHLBI NIH HHS R21 HL093603
6 · The paper itself

Abstract

Mutations in genes that encode for muscle sarcomeric proteins have been identified in humans and two breeds of domestic cats with hypertrophic cardiomyopathy (HCM). This article reviews the history, genetics, and pathogenesis of HCM in the two species in order to give veterinarians a perspective on the genetics of HCM. Hypertrophic cardiomyopathy in people is a genetic disease that has been called a disease of the sarcomere because the preponderance of mutations identified that cause HCM are in genes that encode for sarcomeric proteins (Maron and Maron, 2013). Sarcomeres are the basic contractile units of muscle and thus sarcomeric proteins are responsible for the strength, speed, and extent of muscle contraction. In people with HCM, the two most common genes affected by HCM mutations are the myosin heavy chain gene (MYH7), the gene that encodes for the motor protein β-myosin heavy chain (the sarcomeric protein that splits ATP to generate force), and the cardiac myosin binding protein-C gene (MYBPC3), a gene that encodes for the closely related structural and regulatory protein, cardiac myosin binding protein-C (cMyBP-C). To date, the two mutations linked to HCM in domestic cats (one each in Maine Coon and Ragdoll breeds) also occur in MYBPC3 (Meurs et al., 2005, 2007). This is a review of the genetics of HCM in both humans and domestic cats that focuses on the aspects of human genetics that are germane to veterinarians and on all aspects of feline HCM genetics.

Indexed as

AnimalsCardiomyopathy, HypertrophicCat DiseasesCatsHumansFelineMutationMyosin binding protein C

Identifiers

PMID26776594
PMCPMC5909964
OpenAlexW2250555252

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.