Evidence map›Paper›PMID 28299614›Full record

ReviewCurrent treatment options in cardiovascular medicine2017

Lamin A/C Cardiomyopathies: Current Understanding and Novel Treatment Strategies.

Xi Wang, Allyson Zabell, Wonshill Koh, W H Wilson Tang

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current treatment options in cardiovascular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

24 citing papers in PubMed, 36 citations in OpenAlex.

  1. Trial
  2. DNA damage and repair in cardiomyopathy: mechanisms and therapeutic opportunities.American journal of physiology. Heart and circulatory physiology · 2026
    Review
  3. Review
  4. Targeting Mitochondria Dysfunction in LMNA Cardiomyopathy.JACC. Basic to translational science · 2024
    Article
  5. Review
  6. Characterization of cardiac involvement in children withFrontiers in cell and developmental biology · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Personalized Medicine Approach in a DCM Patient withJournal of personalized medicine · 2022
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Identification of Target Genes and Transcription Factors in Mice with LMNA-Related Dilated Cardiomyopathy by Integrated Bioinformatic Analyses.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  17. Article
  18. Cardiac diseases as a predictor warning of hereditary muscle diseases. The case of laminopathies.Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology · 2019
    Article
  19. Review
  20. Plasma microRNAs as biomarkers for Lamin A/C-related dilated cardiomyopathy.Journal of molecular medicine (Berlin, Germany) · 2018
    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

4 authors at 3 institutions in 1 country.

Xi WangDepartment of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland, OH, USA.
Allyson ZabellDepartment of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland, OH, USA.
Wonshill KohChildren's Hospital of Pittsburgh, Children's Hospital of Pittsburgh, University of Pittsburgh Medical Center, Pittsburgh, PA, USA.
W H Wilson TangDepartment of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland, OH, USA. tangw@ccf.org.
Cleveland Clinic Lerner College of Medicine · USChildren's Hospital of Pittsburgh · USCleveland Clinic · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

opinion statementDilated cardiomyopathy (DCM) is the third leading cause of heart failure in the USA. A major gene associated with DCM with cardiac conduction system disease is lamin A/C (LMNA) gene. Lamins are type V filaments that serve a variety of roles, including nuclear structure support, DNA repair, cell signaling pathway mediation, and chromatin organization. In 1999, LMNA was found responsible for Emery-Dreifuss muscular dystrophy (EDMD) and, since then, has been found in association with a wide spectrum of diseases termed laminopathies, including LMNA cardiomyopathy. Patients with LMNA mutations have a poor prognosis and a higher risk for sudden cardiac death, along with other cardiac effects like dysrhythmias, development of congestive heart failure, and potential need of a pacemaker or ICD. As of now, there is no specific treatment for laminopathies, including LMNA cardiomyopathy, because the mechanism of LMNA mutations in humans is still unclear. This review discusses LMNA mutations and how they relate to DCM, the necessity for further investigation to better understand LMNA mutations, and potential treatment options ranging from clinical and therapeutic to cellular and molecular techniques.

Indexed as

Conduction defectDilated cardiomyopathyLamin A/C cardiomyopathy

Identifiers

PMID28299614
OpenAlexW2598348069

What Socratic holds

Textmetadata
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 Socratic graph.