Evidence map›Paper›PMID 35884947›Full record

ArticleBiomedicines2022

Metformin Is Associated with the Inhibition of Renal Artery AT1R/ET-1/iNOS Axis in a Rat Model of Diabetic Nephropathy with Suppression of Inflammation and Oxidative Stress and Kidney Injury.

Amal F Dawood, Amro Maarouf, Norah M Alzamil, Maha A Momenah, Ayed A Shati, Nervana M Bayoumy, Samaa S Kamar, Mohamed A Haidara, Asmaa M ShamsEldeen, Hanaa Z Yassin and 2 more

Open access · goldAbstract read
In one paragraph

Article in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

17 citing papers in PubMed, 35 citations in OpenAlex.

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  13. Loss of endothelial glucocorticoid receptor accelerates organ fibrosis inAmerican journal of physiology. Renal physiology · 2023
    Article
  14. Loss of endothelial glucocorticoid receptor accelerates organ fibrosis inbioRxiv : the preprint server for biology · 2023
    Article
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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 6 institutions in 3 countries.

Amal F DawoodDepartment of Basic Medical Sciences, College of Medicine, Princess Nourah Bint Abdulrahman University, Riyadh 11671, Saudi Arabia.ORCID 0000-0001-7646-0909
Amro MaaroufDepartment of Clinical Biochemistry, Birmingham Heartlands Hospital, University Hospitals Birmingham NHS Foundation Trust, Birmingham B9 5SS, UK.
Norah M AlzamilDepartment of Clinical Science, Family Medicine, College of Medicine, Princess Nourah Bint Abdulrahman University, Riyadh 11671, Saudi Arabia.
Maha A MomenahDepartment of Biology, College of Science, Princess Nourah Bint Abdulrahman University, Riyadh 11671, Saudi Arabia.ORCID 0000-0002-1827-0995
Ayed A ShatiDepartment of Child Health, College of Medicine, King Khalid University, Abha 62529, Saudi Arabia.ORCID 0000-0003-0444-5595
Nervana M BayoumyDepartment of Physiology, College of Medicine, King Saud University, Riyadh 11461, Saudi Arabia.
Samaa S KamarDepartment of Histology, Kasr Al-Aini Faculty of Medicine, Cairo University, Cairo 12613, Egypt.
Mohamed A HaidaraDepartment of Physiology, Kasr Al-Aini Faculty of Medicine, Cairo University, Cairo 12613, Egypt.ORCID 0000-0003-0990-8093
Asmaa M ShamsEldeenDepartment of Physiology, Kasr Al-Aini Faculty of Medicine, Cairo University, Cairo 12613, Egypt.ORCID 0000-0002-4250-0818
Hanaa Z YassinDepartment of Physiology, Kasr Al-Aini Faculty of Medicine, Cairo University, Cairo 12613, Egypt.
Peter W HewettInstitute of Cardiovascular Sciences, College of Medicine and Dental Sciences, University of Birmingham, Birmingham B15 2TT, UK.
Bahjat Al-AniDepartment of Physiology, College of Medicine, King Khalid University, Abha 62529, Saudi Arabia.
Cairo University · EGPrincess Nourah bint Abdulrahman University · SAKing Khalid University · SAKing Saud University · SAUniversity Hospitals Birmingham NHS Foundation Trust · GBUniversity of Birmingham · GB

Funding

Health Sciences Research Center, King Abdullah bin Abdulaziz University Hospital, Princess Nourah bint Abdulrahman University Research Funding Program, grant No [G18-00006].
6 · The paper itself

Abstract

Diabetes is the most common cause of end-stage renal disease, also called kidney failure. The link between the renal artery receptor angiotensin II type I (AT1R) and endothelin-1 (ET-1), involved in vasoconstriction, oxidative stress, inflammation and kidney fibrosis (collagen) in diabetes-induced nephropathy with and without metformin incorporation has not been previously studied. Diabetes (type 2) was induced in rats and another group started metformin (200 mg/kg) treatment 2 weeks prior to the induction of diabetes and continued on metformin until being culled at week 12. Diabetes significantly (p < 0.0001) modulated renal artery tissue levels of AT1R, ET-1, inducible nitric oxide synthase (iNOS), endothelial NOS (eNOS), and the advanced glycation end products that were protected by metformin. In addition, diabetes-induced inflammation, oxidative stress, hypertension, ketonuria, mesangial matrix expansion, and kidney collagen were significantly reduced by metformin. A significant correlation between the AT1R/ET-1/iNOS axis, inflammation, fibrosis and glycemia was observed. Thus, diabetes is associated with the augmentation of the renal artery AT1R/ET-1/iNOS axis as well as renal injury and hypertension while being protected by metformin.

Indexed as

AT1R/ET-1/iNOS axisdiabetic nephropathykidney fibrosismesangial expansionmetforminrenal artery

Identifiers

PMID35884947
PMCPMC9313150
OpenAlexW4284880053

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.