Evidence map›Paper›PMID 34866995›Full record

ArticleSaudi journal of biological sciences2021

Immunoregulatory effect of mesenchymal stem cell via mitochondria signaling pathways in allergic asthma.

Minmin Huang, Entezar Mehrabi Nasab, Seyyed Shamsadin Athari

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Saudi journal of biological sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

15 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Immune responses and activity of inflammatory mediators in pulmonary vein arrhythmogenesis.International journal of cardiology. Cardiovascular risk and prevention · 2025
    Review
  6. Review
  7. Lung stem cells and respiratory epithelial chimerism in transplantation.European respiratory review : an official journal of the European Respiratory Society · 2025
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Ferroptosis triggers airway inflammation in asthma.Therapeutic advances in respiratory disease
    Review
  15. 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

3 authors at 2 institutions in 1 country.

Minmin HuangDepartment of ICU, People's Hospital of Haimen District, Nantong City, Jiangsu Province, Haimen District, Nantong City, Jiangsu Province 226100, China.
Entezar Mehrabi NasabDepartment of Cardiology, School of Medicine, Tehran Heart Center, Tehran University of Medical Sciences, Tehran, Iran.
Seyyed Shamsadin AthariDepartment of Immunology, School of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran.
Tehran University of Medical Sciences · IRZanjan University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Asthma is a complicated lung disease, which has increased morbidity and mortality rates in worldwide. There is an overlap between asthma pathophysiology and mitochondrial dysfunction and MSCs may have regulatory effect on mitochondrial dysfunction and treats asthma. Therefore, immune-modulatory effect of MSCs and mitochondrial signaling pathways in asthma was studied. After culturing of MSCs and producing asthma animal model, the mice were treated with MSCs via IV via IT. BALf's eosinophil Counting, The levels of IL-4, -5, -13, -25, -33, INF-γ, Cys-LT, LTB4, LTC4, mitochondria genes expression of COX-1, COX-2, ND1, Nrf2, Cytb were measured and lung histopathological study were done. BALf's eosinophils, the levels of IL-4, -5, -13, -25, -33, LTB4, LTC4, Cys-LT, the mitochondria genes expression (COX-1, COX-2, Cytb and ND-1), perivascular and peribronchial inflammation, mucus hyper-production and hyperplasia of the goblet cell in pathological study were significantly decreased in MSCs-treated asthma mice and reverse trend was found about Nrf-2 gene expression, IFN-γ level and ratio of the INF-γ/IL-4. MSC therapy can control inflammation, immune-inflammatory factors in asthma and mitochondrial related genes, and prevent asthma immune-pathology.

Indexed as

AHR, Airway hyperresponsivenessAllergyATP, Adenosine triphosphateBALF, Bronchoalveolar lavage fluidBM, Bone marrowCCL, Chemokine (C-C motif) ligandCD, Cluster of differentiationCOX, CyclooxygenaseCys-LT, Cysteinyl LeukotrieneCytb, Cytochrome bDrp1, Mitochondrial fission depends on the cytosolic GTPase dynamin-related protein 1ELISA, Enzyme-linked immunosorbent assayFIS1, Mitochondrial fission 1 proteinH&E, Haemotoxylin and eosinHGF, Hepatocyte growth factorHLA, Human leukocyte antigenHO, Heme oxygenaseIDO, Indoleamine 2,3-dioxygenaseIFN, InterferonIg, ImmunoglobulinIL, InterleukinImmune systemInflammationIP, Intraperitoneal injectioniPSC, induced pluripotent stem cellsIT, Intratrachea administrationLT, LeukotrieneMFN, MitofusinMIP, macrophage inflammatory proteinMMP, Matrix metalloproteinaseMSCMSC/BI, mesenchymal stem cell bronchial administrationMSC/IV, mesenchymal stem cell intravenous injectionMSC, mesenchymal stem cellND1, NADH-ubiquinone oxidoreductase chain 1NO, Nitric oxideNrf, Nuclear erythroid 2 p45-related factorOPA1, Mitochondrial dynamin like GTPaseOVA, OvalbuminPAS, Periodic-acid-SchiffPBS, Phosphate-buffered salinePGC1a, Peroxisome proliferator-activated receptor gamma coactivator 1-alphaPGE2, Prostaglandin E2ROS, Reactive oxygen speciesTFAM, Transcription factor A mitochondrialTGF, Transforming growth factorTh, T helperTNF, Tumor necrosis factor

Identifiers

PMID34866995
PMCPMC8626264
OpenAlexW3189858372

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.