Evidence map›Paper›PMID 37569832›Full record

ArticleInternational journal of molecular sciences2023

Amniotic Membrane-Derived Stromal Cells Release Extracellular Vesicles That Favor Regeneration of Dystrophic Skeletal Muscles.

Martina Sandonà, Federica Esposito, Anna Cargnoni, Antonietta Silini, Pietro Romele, Ornella Parolini, Valentina Saccone

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Review
  2. Nur77 Regulates the Phosphorylation of Smad3, Thereby Influencing Skeletal Muscle Fibrosis Caused by Obesity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Stem/progenitor cell-based therapy for Duchenne muscular dystrophy.Frontiers in cell and developmental biology · 2025
    Review
  8. 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

7 authors.

Martina SandonàIstituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Fondazione Santa Lucia, Via Fosso di Fiorano 64, 00143 Rome, Italy.ORCID 0000-0001-6732-5756
Federica EspositoIstituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Fondazione Santa Lucia, Via Fosso di Fiorano 64, 00143 Rome, Italy.
Anna CargnoniCentro di Ricerca "E. Menni", Fondazione Poliambulanza Istituto Ospedaliero, 25124 Brescia, Italy.
Antonietta SiliniCentro di Ricerca "E. Menni", Fondazione Poliambulanza Istituto Ospedaliero, 25124 Brescia, Italy.ORCID 0000-0001-6208-3583
Pietro RomeleCentro di Ricerca "E. Menni", Fondazione Poliambulanza Istituto Ospedaliero, 25124 Brescia, Italy.
Ornella ParoliniDepartment of Life Science and Public Health, Università Cattolica del Sacro Cuore, Largo F. Vito 1, 00168 Rome, Italy.ORCID 0000-0002-5211-6430
Valentina SacconeIstituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Fondazione Santa Lucia, Via Fosso di Fiorano 64, 00143 Rome, Italy.

Funding

French Muscular Dystrophy Association 23217PRIN 2017 program of Italian Ministry of Research and University (MIUR) 2017RSAFK7
6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD) is a muscle disease caused by mutations in the dystrophin gene characterized by myofiber fragility and progressive muscle degeneration. The genetic defect results in a reduced number of self-renewing muscle stem cells (MuSCs) and an impairment of their activation and differentiation, which lead to the exhaustion of skeletal muscle regeneration potential and muscle replacement by fibrotic and fatty tissue. In this study, we focused on an unexplored strategy to improve MuSC function and to preserve their niche based on the regenerative properties of mesenchymal stromal cells from the amniotic membrane (hAMSCs), that are multipotent cells recognized to have a role in tissue repair in different disease models. We demonstrate that the hAMSC secretome (CM hAMSC) and extracellular vesicles (EVs) isolated thereof directly stimulate the in vitro proliferation and differentiation of human myoblasts and mouse MuSC from dystrophic muscles. Furthermore, we demonstrate that hAMSC secreted factors modulate the muscle stem cell niche in dystrophic-

Indexed as

Extracellular VesiclesMesenchymal Stem CellsMuscular Dystrophy, DuchenneSatellite Cells, Skeletal MuscleAmnionAnimalsDisease Models, AnimalDystrophinHumansMiceMice, Inbred mdxMuscle, SkeletalDystrophinamnionDuchenne muscular dystrophyextracellular vesiclesmesenchymal stem/stromal cellsskeletal muscle regeneration

Identifiers

PMID37569832
PMCPMC10418925

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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.