Evidence map›Paper›PMID 34706731›Full record

ArticleCell communication and signaling : CCS2021

Perturbation of PI3K/Akt signaling affected autophagy modulation in dystrophin-deficient myoblasts.

Muhammad Dain Yazid, Chen Hung-Chih

Open access · goldAbstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Stem/progenitor cell-based therapy for Duchenne muscular dystrophy.Frontiers in cell and developmental biology · 2025
    Review
  8. Review
  9. The Role of MicroRNA in the Pathogenesis of Duchenne Muscular Dystrophy.International journal of molecular sciences · 2024
    Review
  10. Article
  11. Article
  12. Review
  13. Modelling Skeletal Muscle Ageing and RepairJournal of tissue engineering and regenerative medicine · 2023
    Article
  14. Article
  15. Article
  16. Torin1 restores proliferation rate in Charcot-Marie-Tooth disease type 2A cells harbouring MFN2 (mitofusin 2) mutation.Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology · 2022
    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

2 authors at 2 institutions in 3 countries.

Muhammad Dain YazidCentre for Tissue Engineering and Regenerative Medicine, Faculty of Medicine, UKM Medical Centre, Jalan Yaacob Latiff, 56000, Cheras, Kuala Lumpur, Malaysia. dain@ukm.edu.my.ORCID 0000-0001-6162-4405
Chen Hung-ChihSchool of Biosciences, University of Birmingham, Edgbaston, Birmingham, B15 2TT, UK.
Institute of Sociology, Academia Sinica · TWUniversity Kebangsaan Malaysia Medical Centre · MY

Funding

Universiti Kebangsaan Malaysia GUP-2019-030
6 · The paper itself

Abstract

backgroundThe absence of dystrophin has gave a massive impact on myotube development in Muscular Dystrophy pathogenesis. One of the conserved signaling pathways involved in skeletal muscle differentiation is the PI3K/Akt/mTOR pathway that plays a vital role in autophagy regulation. To further understand and establish targeted therapy in dystrophin-deficient myoblasts, protein expression profiling has been determined which provides information on perturbed autophagy modulation and activation.

methodsIn this study, a dystrophin-deficient myoblast cell line established from the skeletal muscle of a dystrophic (mdx) mouse was used as a model. The dfd13 (dystrophin-deficient) and C2C12 (non-dystrophic) myoblasts were cultured in low mitogen conditions for 10 days to induce differentiation. The cells were subjected to total protein extraction prior to Western blotting assay technique. Protein sub-fractionation has been conducted to determine protein localization. The live-cell analysis of autophagy assay was done using a flow cytometer.

resultsIn our culture system, the dfd13 myoblasts did not achieve terminal differentiation. PTEN expression was profoundly increased in dfd13 myoblasts throughout the differentiation day subsequently indicates perturbation of PI3K/Akt/mTOR regulation. In addition, rictor-mTORC2 was also found inactivated in this event. This occurrence has caused FoxO3 misregulation leads to higher activation of autophagy-related genes in dfd13 myoblasts. Autophagosome formation was increased as LC3B-I/II showed accumulation upon differentiation. However, the ratio of LC3B lipidation and autophagic flux were shown decreased which exhibited dystrophic features.

conclusionPerturbation of the PTEN-PI3K/Akt pathway triggers excessive autophagosome formation and subsequently reduced autophagic flux within dystrophin-deficient myoblasts where these findings are of importance to understand Duchenne Muscular Dystrophy (DMD) patients. We believe that some manipulation within its regulatory signaling reported in this study could help restore muscle homeostasis and attenuate disease progression. Video Abstract.

Indexed as

AnimalsAutophagyCell DifferentiationClass I Phosphatidylinositol 3-KinasesDisease Models, AnimalDystrophinFlow CytometryForkhead Box Protein O3HumansMiceMice, Inbred mdxMicrotubule-Associated ProteinsMuscle Fibers, SkeletalMuscular Dystrophy, DuchenneMyoblastsProto-Oncogene Proteins c-aktClass I Phosphatidylinositol 3-KinasesDmd protein, mouseDystrophinForkhead Box Protein O3FoxO3 protein, mouseMap1lc3b protein, mouseMicrotubule-Associated ProteinsPik3cd protein, mouseProto-Oncogene Proteins c-aktRapamycin-Insensitive Companion of mTOR Proteinrictor protein, mouseTOR Serine-Threonine KinasesAutophagyDuchenne muscular dystrophyDystrophinMyoblastsPI3K/Akt signalling

Identifiers

PMID34706731
PMCPMC8554905
OpenAlexW3107320558

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.