Evidence map›Paper›PMID 37502180›Full record

ArticleFrontiers in cardiovascular medicine2023

Ameliorating diabetes-associated atherosclerosis and diabetic nephropathy through modulation of soluble guanylate cyclase.

Arpeeta Sharma, Judy Choi, Lachlan Sim, Abhiroop Dey, Muthukumar Mohan, Phillip Kantharidis, Lisa Dietz, Peter Sandner, Judy B de Haan

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cardiovascular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

7 citing papers in PubMed, 9 citations in OpenAlex.

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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

9 authors at 5 institutions in 2 countries.

Arpeeta SharmaCardiovascular Inflammation and Redox Biology Laboratory, Baker Heart and Diabetes Institute, Melbourne, VIC, Australia.
Judy ChoiCardiovascular Inflammation and Redox Biology Laboratory, Baker Heart and Diabetes Institute, Melbourne, VIC, Australia.
Lachlan SimCardiovascular Inflammation and Redox Biology Laboratory, Baker Heart and Diabetes Institute, Melbourne, VIC, Australia.
Abhiroop DeyCardiovascular Inflammation and Redox Biology Laboratory, Baker Heart and Diabetes Institute, Melbourne, VIC, Australia.
Muthukumar MohanDepartment of Diabetes, Monash University, Central Clinical School, Melbourne, VIC, Australia.
Phillip KantharidisDepartment of Diabetes, Monash University, Central Clinical School, Melbourne, VIC, Australia.
Lisa DietzPharmaceuticals Research and Development, Bayer AG, Wuppertal, Germany.
Peter SandnerPharmaceuticals Research and Development, Bayer AG, Wuppertal, Germany.
Judy B de HaanCardiovascular Inflammation and Redox Biology Laboratory, Baker Heart and Diabetes Institute, Melbourne, VIC, Australia.
Baker Heart and Diabetes Institute · AUMonash University · AUBayer (Germany) · DELa Trobe University · AUMedizinische Hochschule Hannover · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes mellitus (DM) is an independent risk factor for micro- and macrovascular complications such as nephropathy and atherosclerosis respectively, which are the major causes of premature morbidity and mortality in Type 1 and Type 2 diabetic patients. Endothelial dysfunction is the critical first step of vascular disease and is characterized by reduced bioavailability of the essential endothelial vasodilator, nitric oxide (NO), coupled with an elevation in inflammation and oxidative stress. A novel pathway to bolster NO activity is to upregulate soluble guanylate cyclase (sGC), an enzyme responsible for mediating the protective actions of NO. Two classes of sGC modulators exist, activators and stimulators, with differing sensitivity to oxidative stress. In this study, we investigated the therapeutic effects of the sGC stimulator BAY 41-2272 (Bay 41) and the sGC activator BAY 60-2770 (Bay 60) on endpoints of atherosclerosis and renal disease as well as inflammation and oxidative stress in diabetic Apolipoprotein E knockout (ApoE-/-) mice. We hypothesized that under oxidative conditions known to accompany diabetes, sGC activation might be more efficacious than sGC stimulation in limiting diabetic vascular complications. We demonstrate that Bay 60 not only significantly decreased nitrotyrosine staining (

Indexed as

atherosclerosisendothelial dysfunctioninflammationnitric oxideoxidative stresssoluble guanylate cyclasetype 2 diabetes

Identifiers

PMID37502180
PMCPMC10368983
OpenAlexW4384024652

What OpenQuestion holds

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LicenceCC BY
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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.