Evidence mapPaperPMID 35876284Full record

ReviewAmerican journal of physiology. Cell physiology2022

A glitch in the matrix: the pivotal role for extracellular matrix remodeling during muscle hypertrophy.

Camille R Brightwell, Christine M Latham, Nicholas T Thomas, Alexander R Keeble, Kevin A Murach, Christopher S Fry

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Cell physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05879575 (Effects and Pathophysiology of Weight Training on Pregnancy-related Pelvic Girdle Pain), which is not on this map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.7field-weighted citation impact, top 5% 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.

NCT05879575 naunknown statusnot on this mapstarted 2023, after this paper: background citation

Effects and Pathophysiology of Weight Training on Pregnancy-related Pelvic Girdle Pain (PPGP)

TypeinterventionalSponsorNational Taiwan University Hospital Hsin-Chu BranchRan2023 to 2024Enrolled70ConditionsPelvic Girdle PainArmsweight training
3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 46 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

6 authors at 2 institutions in 1 country.

Camille R BrightwellCenter for Muscle Biology, University of Kentucky, Lexington, Kentucky.
Christine M LathamCenter for Muscle Biology, University of Kentucky, Lexington, Kentucky.
Nicholas T ThomasCenter for Muscle Biology, University of Kentucky, Lexington, Kentucky.ORCID 0000-0003-4578-8463
Alexander R KeebleCenter for Muscle Biology, University of Kentucky, Lexington, Kentucky.
Kevin A MurachDepartment of Health, Human Performance, and Recreation, Molecular Muscle Mass Regulation Laboratory, Exercise Science Research Center, University of Arkansas, Fayetteville, Arkansas.
Christopher S FryCenter for Muscle Biology, University of Kentucky, Lexington, Kentucky.ORCID 0000-0002-4207-6594
University of Kentucky · USUniversity of Arkansas at Fayetteville · US

Funding

Myostatin Alters Muscle Composition as The Result of an ACL InjuryR01AR072061 · NIAMS · UNIVERSITY OF KENTUCKY · PI Christopher Fry · 2023 to 2023
$435k
NIAMS NIH HHS R01 AR072061NIA NIH HHS R00 AG063994
6 · The paper itself

Abstract

Multinuclear muscle fibers are the most voluminous cells in skeletal muscle and the primary drivers of growth in response to loading. Outside the muscle fiber, however, is a diversity of mononuclear cell types that reside in the extracellular matrix (ECM). These muscle-resident cells are exercise-responsive and produce the scaffolding for successful myofibrillar growth. Without proper remodeling and maintenance of this ECM scaffolding, the ability to mount an appropriate response to resistance training in adult muscles is severely hindered. Complex cellular choreography takes place in muscles following a loading stimulus. These interactions have been recently revealed by single-cell explorations into muscle adaptation with loading. The intricate ballet of ECM remodeling involves collagen production from fibrogenic cells and ECM modifying signals initiated by satellite cells, immune cells, and the muscle fibers themselves. The acellular collagen-rich ECM is also a mechanical signal-transducer and rich repository of growth factors that may directly influence muscle fiber hypertrophy once liberated. Collectively, high levels of collagen expression, deposition, and turnover characterize a well-trained muscle phenotype. The purpose of this review is to highlight the most recent evidence for how the ECM and its cellular components affect loading-induced muscle hypertrophy. We also address how the muscle fiber may directly take part in ECM remodeling, and whether ECM dynamics are rate limiting for muscle fiber growth.

Indexed as

Extracellular MatrixMuscle Fibers, SkeletalCollagenHumansHypertrophyMuscle, SkeletalCollagencollagenfibro/adipogenic progenitorsmechanical overloadsatellite cellsskeletal muscle

Identifiers

PMID35876284
PMCPMC9448331
OpenAlexW4287307852

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

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.