Evidence map›Paper›PMID 23966782›Full record

ArticleInternational journal of nanomedicine2013

Nanolipodendrosome-loaded glatiramer acetate and myogenic differentiation 1 as augmentation therapeutic strategy approaches in muscular dystrophy.

Ehsan Afzal, Saba Zakeri, Peyman Keyhanvar, Meisam Bagheri, Parvin Mahjoubi, Mahtab Asadian, Nogol Omoomi, Mohammad Dehqanian, Negar Ghalandarlaki, Tahmineh Darvishmohammadi and 7 more

Open access · goldAbstract read
In one paragraph

Article in International journal of nanomedicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.1field-weighted citation impact, top 43% 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

6 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Nanotherapy for Duchenne muscular dystrophy.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnology · 2018
    Review
  6. Nanomedicine Therapies for Pediatric Diseases.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnology
    Review
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

17 authors at 8 institutions in 2 countries.

Ehsan AfzalDepartment of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran.
Saba Zakeri
Peyman Keyhanvar
Meisam Bagheri
Parvin Mahjoubi
Mahtab Asadian
Nogol Omoomi
Mohammad Dehqanian
Negar Ghalandarlaki
Tahmineh Darvishmohammadi
Fatemeh Farjadian
Mohammad Sadegh Golvajoee
Shadi Afzal
Maryam Ghaffari
Reza Ahangari Cohan
Amin Gravand
Mehdi Shafiee Ardestani
Islamic Azad University, Science and Research Branch · IRPasteur Institute of Iran · IRTehran University of Medical Sciences · IRAhvaz Jundishapur University of Medical Sciences · IRIslamic Azad University Pharmaceutical Sciences Branch · IRIslamic Azad University, Tehran · IRShiraz University · IRShiraz University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background[Corrected] Muscular dystrophies consist of a number of juvenile and adult forms of complex disorders which generally cause weakness or efficiency defects affecting skeletal muscles or, in some kinds, other types of tissues in all parts of the body are vastly affected. In previous studies, it was observed that along with muscular dystrophy, immune inflammation was caused by inflammatory cells invasion - like T lymphocyte markers (CD8+/CD4+). Inflammatory processes play a major part in muscular fibrosis in muscular dystrophy patients. Additionally, a significant decrease in amounts of two myogenic recovery factors (myogenic differentation 1 [MyoD] and myogenin) in animal models was observed. The drug glatiramer acetate causes anti-inflammatory cytokines to increase and T helper (Th) cells to induce, in an as yet unknown mechanism. MyoD recovery activity in muscular cells justifies using it alongside this drug.

methodsIn this study, a nanolipodendrosome carrier as a drug delivery system was designed. The purpose of the system was to maximize the delivery and efficiency of the two drug factors, MyoD and myogenin, and introduce them as novel therapeutic agents in muscular dystrophy phenotypic mice. The generation of new muscular cells was analyzed in SW1 mice. Then, immune system changes and probable side effects after injecting the nanodrug formulations were investigated.

resultsThe loaded lipodendrimer nanocarrier with the candidate drug, in comparison with the nandrolone control drug, caused a significant increase in muscular mass, a reduction in CD4+/CD8+ inflammation markers, and no significant toxicity was observed. The results support the hypothesis that the nanolipodendrimer containing the two candidate drugs will probably be an efficient means to ameliorate muscular degeneration, and warrants further investigation.

Indexed as

AnimalsBody WeightCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesGlatiramer AcetateLiposomesMaleMiceMicroscopy, Electron, TransmissionMuscle, SkeletalMuscular DystrophiesMyoD ProteinNandroloneNanoparticlesParticle SizePeptidesGlatiramer AcetateLiposomesMyoD1 myogenic differentiation proteinMyoD ProteinNandrolonePeptidesdrug deliveryglatiramer acetatemuscular dystrophyMyoD factor

Identifiers

PMID23966782
PMCPMC3743640
OpenAlexW2035102199

What OpenQuestion holds

Textmetadata
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.