Evidence map›Paper›PMID 32887916›Full record

ArticleScientific reports2020

Canagliflozin ameliorates renal oxidative stress and inflammation by stimulating AMPK-Akt-eNOS pathway in the isoprenaline-induced oxidative stress model.

Raquibul Hasan, Shoumen Lasker, Ahasanul Hasan, Farzana Zerin, Mushfera Zamila, Faisal Parvez, Md Mizanur Rahman, Ferdous Khan, Nusrat Subhan, Md Ashraful Alam

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

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
9.7field-weighted citation impact, top 1% 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

62 citing papers in PubMed, 106 citations in OpenAlex.

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  11. The interaction between dysfunction of vasculature and tauopathy in Alzheimer's disease and related dementias.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
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2 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

10 authors at 2 institutions in 2 countries.

Raquibul HasanDepartment of Pharmaceutical Sciences, College of Pharmacy, Mercer University Health Sciences Center, Mercer University, Atlanta, GA, 30341, USA. hasan_r@mercer.edu.
Shoumen LaskerDepartment of Pharmaceutical Sciences, North South University, Bashundhara, Dhaka, 1229, Bangladesh.
Ahasanul HasanDepartment of Pharmaceutical Sciences, College of Pharmacy, Mercer University Health Sciences Center, Mercer University, Atlanta, GA, 30341, USA.
Farzana ZerinDepartment of Pharmaceutical Sciences, College of Pharmacy, Mercer University Health Sciences Center, Mercer University, Atlanta, GA, 30341, USA.
Mushfera ZamilaDepartment of Pharmaceutical Sciences, North South University, Bashundhara, Dhaka, 1229, Bangladesh.
Faisal ParvezDepartment of Pharmaceutical Sciences, North South University, Bashundhara, Dhaka, 1229, Bangladesh.
Md Mizanur RahmanDepartment of Pharmaceutical Sciences, North South University, Bashundhara, Dhaka, 1229, Bangladesh.
Ferdous KhanDepartment of Pharmaceutical Sciences, North South University, Bashundhara, Dhaka, 1229, Bangladesh.
Nusrat SubhanDepartment of Pharmaceutical Sciences, North South University, Bashundhara, Dhaka, 1229, Bangladesh.
Md Ashraful AlamDepartment of Pharmaceutical Sciences, North South University, Bashundhara, Dhaka, 1229, Bangladesh. ashraful.alam@northsouth.edu.
North South University · BDMercer University Health Sciences Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes is a leading cause of chronic kidney disease, and the high prevalence of sympathetic nervous system (SNS) hyperactivity in diabetic patients makes them further susceptible to SNS-mediated oxidative stress and accelerated kidney damage. Here, we investigated if canagliflozin can reverse isoprenaline (ISO)-induced renal oxidative damage in rats, a model that mimics SNS overstimulation-induced organ injuries in humans. We found that ISO administration elevates renal oxidative stress markers including malondialdehyde (MDA), advanced protein oxidation product (APOP), myeloperoxidase (MPO) and nitric oxide (NO), while depleting levels of endogenous antioxidants such as catalase (CAT), superoxide dismutase (SOD) and glutathione (GSH). Strikingly, canagliflozin treatment of ISO-treated rats not only prevents elevation of oxidative stress markers but also rescues levels of depleted antioxidants. Our results also show that canagliflozin stimulates antioxidant/anti-inflammatory signaling pathways involving AMP-activated protein kinase (AMPK), Akt and eNOS, and inhibits iNOS and NADPH oxidase isoform 4 (NOX4), all of which are associated with oxidative stress and inflammation. Further, canagliflozin prevents ISO-induced apoptosis of kidney cells by inhibiting Bax protein upregulation and caspase-3 activation. Histological examination of kidney sections reveal that canagliflozin attenuates ISO-mediated increases in inflammatory cell infiltration, collagen deposition and fibrosis. Finally, consistent with these findings, canagliflozin treatment improves kidney function in ISO-treated rats, suggesting that the antioxidant effects may be clinically translatable.

Indexed as

AMP-Activated Protein KinasesAnimalsAnti-Inflammatory AgentsAntioxidantsCanagliflozinCells, CulturedDisease Models, AnimalEpithelial CellsHumansInflammationIsoproterenolKidney TubulesMaleNitric Oxide Synthase Type IIIOxidative StressProto-Oncogene Proteins c-aktAMP-Activated Protein KinasesAnti-Inflammatory AgentsAntioxidantsCanagliflozinIsoproterenolNitric Oxide Synthase Type IIINOS3 protein, humanNos3 protein, ratProto-Oncogene Proteins c-akt

Identifiers

PMID32887916
PMCPMC7474058
OpenAlexW3083174088

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.