Evidence map›Paper›PMID 31443395›Full record

ReviewInternational journal of molecular sciences2019

Cardiac Pathophysiology and the Future of Cardiac Therapies in Duchenne Muscular Dystrophy.

Tatyana A Meyers, DeWayne Townsend

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 2 pooled it
6.3field-weighted citation impact, top 3% 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

70 citing papers in PubMed, 2 syntheses or guidelines pooled it, 132 citations in OpenAlex.

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  18. Mechanisms of reduced myocardial energetics of the dystrophic heart.American journal of physiology. Heart and circulatory physiology · 2024
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10 more citing papers are in PubMed but not listed here.

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.

Tatyana A MeyersDepartment of Integrative Biology and Physiology, Medical School, University of Minnesota, Minneapolis, MN 55455, USA.ORCID 0000-0002-9904-9140
DeWayne TownsendDepartment of Integrative Biology and Physiology, Medical School, University of Minnesota, Minneapolis, MN 55455, USA. town0045@umn.edu.
University of Minnesota Medical Center · US

Funding

Female Resilience in Dystrophic CardiomyopathyF31HL139093 · NHLBI · UNIVERSITY OF MINNESOTA · PI VETTER, TATYANA A · 2017 to 2019
$71k
NHLBI NIH HHS F31 HL139093NIH HHS F31-139093NIH HHS R01-HL114832
6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD) is a devastating disease featuring skeletal muscle wasting, respiratory insufficiency, and cardiomyopathy. Historically, respiratory failure has been the leading cause of mortality in DMD, but recent improvements in symptomatic respiratory management have extended the life expectancy of DMD patients. With increased longevity, the clinical relevance of heart disease in DMD is growing, as virtually all DMD patients over 18 year of age display signs of cardiomyopathy. This review will focus on the pathophysiological basis of DMD in the heart and discuss the therapeutic approaches currently in use and those in development to treat dystrophic cardiomyopathy. The first section will describe the aspects of the DMD that result in the loss of cardiac tissue and accumulation of fibrosis. The second section will discuss cardiac small molecule therapies currently used to treat heart disease in DMD, with a focus on the evidence supporting the use of each drug in dystrophic patients. The final section will outline the strengths and limitations of approaches directed at correcting the genetic defect through dystrophin gene replacement, modification, or repair. There are several new and promising therapeutic approaches that may protect the dystrophic heart, but their limitations suggest that future management of dystrophic cardiomyopathy may benefit from combining gene-targeted therapies with small molecule therapies. Understanding the mechanistic basis of dystrophic heart disease and the effects of current and emerging therapies will be critical for their success in the treatment of patients with DMD.

Indexed as

AnimalsCalciumCardiomyopathiesDisease ManagementDisease SusceptibilityDystrophinExonsFibrosisGenetic TherapyHumansMitochondriaMolecular Targeted TherapyMuscular Dystrophy, DuchenneNitric OxideReactive Oxygen SpeciesCalciumDystrophinNitric OxideReactive Oxygen SpeciesDuchenne muscular dystrophydystrophic cardiomyopathyexon skippingfibrosisgene therapyheart disease

Identifiers

PMID31443395
PMCPMC6747383
OpenAlexW2969770826

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.