Evidence map›Paper›PMID 30099631›Full record

ReviewPflugers Archiv : European journal of physiology2019

Unraveling obscurins in heart disease.

Alyssa Grogan, Aikaterini Kontrogianni-Konstantopoulos

Open access · greenAbstract readReview
In one paragraph

Review in Pflugers Archiv : European journal of physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. ALPK2 prevents cardiac diastolic dysfunction in heart failure with preserved ejection fraction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  9. Article
  10. Article
  11. Age and Sex Differences in the Genetics of Cardiomyopathy.Journal of cardiovascular translational research · 2023
    Article
  12. PK1 fromOpen biology · 2023
    Article
  13. Article
  14. Alterations in cytoskeletal and CaFrontiers in cardiovascular medicine · 2023
    Article
  15. Article
  16. Article
  17. Article
  18. Obscurin: A multitasking giant in the fight against cancer.Biochimica et biophysica acta. Reviews on cancer · 2021
    Review
  19. Exploring Obscurin and SPEG Kinase Biology.Journal of clinical medicine · 2021
    Article
  20. 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.

Alyssa GroganDepartment of Biochemistry and Molecular Biology, University of Maryland School of Medicine, 108 N. Greene St., Baltimore, MD, 21201, USA.
Aikaterini Kontrogianni-KonstantopoulosDepartment of Biochemistry and Molecular Biology, University of Maryland School of Medicine, 108 N. Greene St., Baltimore, MD, 21201, USA. akontrogianni@som.umaryland.edu.ORCID 0000-0003-3948-1959
University of Maryland, Baltimore · US

Funding

Interdisciplinary Training Program Muscle BiologyT32AR007592 · NIAMS · UNIVERSITY OF MARYLAND BALTIMORE · PI Aikaterini Kontrogianni-Konstantopoulos · 1996 to 2026
$11.7M
American Heart Association-American Stroke Association 16GRNT31290010NIAMS NIH HHS T32 AR007592NIH HHS T32AR7592
6 · The paper itself

Abstract

Obscurins, expressed from the single OBSCN gene, are a family of giant, modular, cytoskeletal proteins that play key structural and regulatory roles in striated muscles. They were first implicated in the development of heart disease in 2007 when two missense mutations were found in a patient diagnosed with hypertrophic cardiomyopathy (HCM). Since then, the discovery of over a dozen missense, frameshift, and splicing mutations that are linked to various forms of cardiomyopathy, including HCM, dilated cardiomyopathy (DCM), and left ventricular non-compaction (LVNC), has highlighted OBSCN as a potential disease-causing gene. At this time, the functional consequences of the identified mutations remain largely elusive, and much work has yet to be done to characterize the disease mechanisms of pathological OBSCN variants. Herein, we describe the OBSCN mutations known to date, discuss their potential impact on disease development, and provide future directions in order to better understand the involvement of obscurins in heart disease.

Indexed as

MutationAnimalsCardiomyopathy, DilatedCardiomyopathy, HypertrophicHumansProtein Serine-Threonine KinasesRho Guanine Nucleotide Exchange FactorsOBSCN protein, humanProtein Serine-Threonine KinasesRho Guanine Nucleotide Exchange FactorsCardiomyopathyHeart failureObscurinSarcomeric mutations

Identifiers

PMID30099631
PMCPMC6397709
OpenAlexW2885240581

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.