Evidence map›Paper›PMID 37746696›Full record

ReviewAmerican journal of physiology. Cell physiology2023

Extracellular matrix contribution to disease progression and dysfunction in myopathy.

Ashlee M Long, GaHyun Lee, Alexis R Demonbreun, Elizabeth M McNally

Open access · hybridAbstract readReview
In one paragraph

Review in American journal of physiology. Cell physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. The two faces of mitochondrial CaJournal of physiology and biochemistry · 2026
    Review
  5. Article
  6. Article
  7. Article
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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

4 authors at 1 institution in 1 country.

Ashlee M LongCenter for Genetic Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States.
GaHyun LeeCenter for Genetic Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States.
Alexis R DemonbreunCenter for Genetic Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States.
Elizabeth M McNallyCenter for Genetic Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States.ORCID 0000-0002-1221-719X
Northwestern University · US

Funding

Training and education CoreU54AR052646 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI MCNALLY, ELIZABETH M, SWEENEY, H LEE · 2005 to 2020
$24.1M
SARCOGLYCAN IN MYOPATHY AND MUSCLE MEMBRANE STABILITYR01HL061322 · NHLBI · UNIVERSITY OF CHICAGO · PI MCNALLY, ELIZABETH M · 1999 to 2022
$7.5M
Myoferlin in Muscle Membrane Fusion and RepairR01NS047726 · NINDS · UNIVERSITY OF CHICAGO · PI ALEXIS R. DEMONBREUN, Elizabeth M McNally · 2003 to 2026
$7.2M
Understanding and Improving Therapies for the Muscular Dystrophies through Noninvasive BiomarkersP50AR052646 · NIAMS · UNIVERSITY OF FLORIDA · PI WALTER, GLENN · 2021 to 2024
$6.2M
Extracellular matrix regulation of cellular crosstalk in cardiac fibrosisR01HL167813 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI ALEXIS R. DEMONBREUN, Elizabeth M McNally · 2023 to 2026
$2.8M
Development of anti-LTBP4 as a biologic to treat Neuromuscular DiseasesUG3NS127383 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI DEMONBREUN, ALEXIS R., MCNALLY, ELIZABETH M · 2022 to 2023
$2.1M
Northwestern University Molecular and Translational Cardiovascular Training ProgramT32HL134633 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MCNALLY, ELIZABETH M · 2017 to 2021
$1.6M
NHLBI NIH HHS R01 HL061322NHLBI NIH HHS R01 HL167813NHLBI NIH HHS T32 HL134633NIAMS NIH HHS P50 AR052646NIAMS NIH HHS U54 AR052646NINDS NIH HHS R01 NS047726NINDS NIH HHS UG3 NS127383
6 · The paper itself

Abstract

Myopathic processes affect skeletal muscle and heart. In the muscular dystrophies, which are a subset of myopathies, muscle cells are gradually replaced by fibrosis and fat, impairing muscle function as well as regeneration and repair. In addition to skeletal muscle, these genetic disorders often also affect the heart, where fibrofatty infiltration progressively accumulates in the myocardium, impairing heart function. Although considerable effort has focused on gene-corrective and gene-replacement approaches to stabilize myofibers and cardiomyocytes, the continual and ongoing deposition of extracellular matrix itself contributes to tissue and organ dysfunction. Transcriptomic and proteomic profiling, along with high-resolution imaging and biophysical measurements, have been applied to define extracellular matrix components and their role in contributing to cardiac and skeletal muscle weakness. More recently, decellularization methods have been adapted to an on-slide format to preserve the spatial geography of the extracellular matrix, allowing new insight into matrix remodeling and its direct role in suppressing regeneration in muscle. This review highlights recent literature with focus on the extracellular matrix and molecular mechanisms that contribute to muscle and heart fibrotic disorders. We will also compare how the myopathic matrix differs from healthy matrix, emphasizing how the pathological matrix contributes to disease.

Indexed as

Heart DiseasesMuscular DiseasesDisease ProgressionExtracellular MatrixFibrosisHumansMuscle, SkeletalMyocytes, CardiacProteomicsacellular myoscaffoldsdecellularizationfibrosisheartmuscle

Identifiers

PMID37746696
PMCPMC10855263
OpenAlexW4387002635

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.