Evidence map›Paper›PMID 30467302›Full record

ArticleCells2018

Mesenchymal Stem Cell-Derived Exosomes Ameliorated Diabetic Nephropathy by Autophagy Induction through the mTOR Signaling Pathway.

Nesrine Ebrahim, Inas A Ahmed, Noha I Hussien, Arigue A Dessouky, Ayman Samir Farid, Amal M Elshazly, Ola Mostafa, Walaa Bayoumie El Gazzar, Safwa M Sorour, Yasmin Seleem and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
144citing papers in PubMed, 4 pooled it
7.5field-weighted citation impact, top 2% 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

144 citing papers in PubMed, 4 syntheses or guidelines pooled it, 232 citations in OpenAlex.

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84 more citing papers are in PubMed but not listed here.

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

12 authors at 3 institutions in 1 country.

Nesrine EbrahimDepartment of Histology and Cell Biology, Faculty of Medicine, Benha University, Benha 13518, QG, Egypt. nesrien.salem@fmed.bu.edu.eg.
Inas A AhmedDepartment of Medical Biochemistry, Faculty of Medicine, Benha University, Benha 13518, QG, Egypt. inas.ahmed@fmed.bu.edu.eg.
Noha I HussienDepartment of Physiology, Faculty of Medicine, Benha University, Benha 13518, QG, Egypt. drnohaibrahim79@gmail.com.
Arigue A DessoukyDepartment of Histology and Cell Biology, Faculty of Medicine, Zagazig University, Zagazig 44519, Egypt. arigueamir@yahoo.com.
Ayman Samir FaridDepartment of Clinical Pathology, Faculty of Veterinary Medicine, Benha University, Moshtohor, Toukh 13736, QG, Egypt. ayman.samir@fvtm.bu.edu.eg.ORCID 0000-0002-7844-7967
Amal M ElshazlyDepartment of Anatomy, Faculty of Medicine, Benha University, Benha 13518, QG, Egypt. Amal.elshazly79@yahoo.com.
Ola MostafaDepartment of Histology and Cell Biology, Faculty of Medicine, Benha University, Benha 13518, QG, Egypt. ola.mostafa.moez@gmail.com.
Walaa Bayoumie El GazzarDepartment of Medical Biochemistry, Faculty of Medicine, Benha University, Benha 13518, QG, Egypt. bioch_2004@yahoo.com.
Safwa M SorourDepartment of Clinical Pharmacology, Faculty of Medicine, Benha University, Benha 13518, QG, Egypt. safwa.sorour@fmed.bu.edu.eg.
Yasmin SeleemDepartment of Clinical Pharmacology, Faculty of Medicine, Benha University, Benha 13518, QG, Egypt. yasmeen.seleem@fmed.bu.edu.eg.
Ahmed M HusseinDepartment of Internal Medicine, Faculty of Medicine, Benha University, Benha 13518, QG, Egypt. drdabour@yahoo.com.
Dina SabryDepartment of Medical Biochemistry, Faculty of Medicine, Cairo University, Cairo 11562, Egypt. dinasabry@kasralainy.edu.eg.ORCID 0000-0002-6720-3385
Benha University · EGCairo University · EGZagazig University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiabetic nephropathy (DN) is a serious complication of diabetes mellitus and a common cause of end-stage renal disease. Autophagy has a defensive role against kidney damage caused by hyperglycemia. Mesenchymal stem cell (MSC)-derived exosomes are currently considered as a new promising therapy for chronic renal injury. However, the renal-protective mechanism of exosomes on DN is not completely understood. We examined the potential role of MSC-derived exosomes for enhancement of autophagy activity and their effect on DN. In our study, we used five groups of rats: control; DN; DN treated with exosomes; DN treated with 3-methyladenine (3-MA) and chloroquine (inhibitors of autophagy); and DN treated with 3-methyladenine (3-MA), chloroquine, and exosome groups. We assessed renal function, morphology, and fibrosis. Moreover, ratios of the autophagy markers mechanistic target of rapamycin (mTOR), Beclin-1, light chain-3 (LC3-II), and LC3-II/LC3-I were detected. Additionally, electron microscopy was used for detection of autophagosomes.

resultsExosomes markedly improved renal function and showed histological restoration of renal tissues, with significant increase of LC3 and Beclin-1, and significant decrease of mTOR and fibrotic marker expression in renal tissue. All previous effects were partially abolished by the autophagy inhibitors chloroquine and 3-MA.

conclusionWe conclude that autophagy induction by exosomes could attenuate DN in a rat model of streptozotocin-induced diabetes mellitus.

Indexed as

autophagydiabetic nephropathyexosomesmTOR

Identifiers

PMID30467302
PMCPMC6315695
OpenAlexW2892219454

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.