Evidence map›Paper›PMID 33188007›Full record

ArticleDisease models & mechanisms2020

Duchenne muscular dystrophy (DMD) cardiomyocyte-secreted exosomes promote the pathogenesis of DMD-associated cardiomyopathy.

Melanie Gartz, Chien-Wei Lin, Mark A Sussman, Michael W Lawlor, Jennifer L Strande

Open access · goldAbstract read
In one paragraph

Article in Disease models & mechanisms, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Melanie GartzCardiovascular Research Center, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Chien-Wei LinDivision of Biostatistics, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Mark A SussmanSan Diego Heart Institute and Biology Department, San Diego State University, San Diego, CA 92182, USA.ORCID http://orcid.org/0000-0002-0104-4799
Michael W LawlorDepartment of Pathology and Laboratory Medicine, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Jennifer L StrandeCardiovascular Research Center, Medical College of Wisconsin, Milwaukee, WI 53226, USA jstrandemcw@gmail.com.ORCID http://orcid.org/0000-0002-5918-230X
Medical College of Wisconsin · USSan Diego State University · US

Funding

Developing nicorandil and companion biomarkers for DMD cardiomyopathy therapyR01HL134932 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI LAWLOR, MICHAEL WILLIAM · 2017 to 2020
$1.8M
NHLBI NIH HHS R01 HL134932
6 · The paper itself

Abstract

Cardiomyopathy is a leading cause of early mortality in Duchenne muscular dystrophy (DMD). There is a need to gain a better understanding of the molecular pathogenesis for the development effective therapies. Exosomes (exo) are secreted vesicles and exert effects via their RNA, lipid and protein cargo. The role of exosomes in disease pathology is unknown. Exosomes derived from stem cells have demonstrated cardioprotection in the murine DMD heart. However, it is unknown how the disease status of the donor cell type influences exosome function. Here, we sought to determine the phenotypic responses of DMD cardiomyocytes (DMD-iCMs) after long-term exposure to DMD cardiac exosomes (DMD-exo). DMD-iCMs were vulnerable to stress, evidenced by production of reactive oxygen species, the mitochondrial membrane potential and cell death levels. Long-term exposure to non-affected exosomes (N-exo) was protective. By contrast, long-term exposure to DMD-exo was not protective, and the response to stress improved with inhibition of DMD-exo secretion

Indexed as

AnimalsCardiomyopathiesCardiotonic AgentsCell DeathCell LineExosomesFemaleHumansMice, Inbred C57BLMicroRNAsMuscular Dystrophy, DuchenneMyocytes, CardiacParacrine CommunicationProteomeStress, PhysiologicalTranscription, GeneticCardiotonic AgentsMicroRNAsProteomeCardiomyocyteCardiomyopathyExosomeMicroRNAStressVesicle

Identifiers

PMID33188007
PMCPMC7673361
OpenAlexW3100186668

What OpenQuestion holds

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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.