Evidence map›Paper›PMID 29515457›Full record

ReviewFrontiers in physiology2018

Oxidative Stress and NLRP3-Inflammasome Activity as Significant Drivers of Diabetic Cardiovascular Complications: Therapeutic Implications.

Arpeeta Sharma, Mitchel Tate, Geetha Mathew, James E Vince, Rebecca H Ritchie, Judy B de Haan

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

Review in Frontiers in physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed, 2 pooled it
8.9field-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

114 citing papers in PubMed, 2 syntheses or guidelines pooled it, 208 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
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  5. Review
  6. Electrostatic lipidopathy drives human diabetic heart failure.Cardiovascular diabetology. Endocrinology reports · 2026
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  16. Mitigation of nicotine-induced podocyte injury through inhibition of thioredoxin interacting protein.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025
    Article
  17. Review
  18. Rutin: a pain-relieving flavonoid.Inflammopharmacology · 2025
    Review
  19. Review
  20. Review

54 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

6 authors at 3 institutions in 1 country.

Arpeeta SharmaOxidative Stress Laboratory, Basic Science Domain, Baker Heart and Diabetes Institute, Melbourne, VIC, Australia.
Mitchel TateHeart Failure Pharmacology Laboratory, Basic Science Domain, Baker Heart and Diabetes Institute, Melbourne, VIC, Australia.
Geetha MathewCellular Therapies Laboratory, Westmead Hospital, Sydney, NSW, Australia.
James E VinceInflammation Division, Walter and Eliza Hall Institute, Melbourne, VIC, Australia.
Rebecca H RitchieHeart Failure Pharmacology Laboratory, Basic Science Domain, Baker Heart and Diabetes Institute, Melbourne, VIC, Australia.
Judy B de HaanOxidative Stress Laboratory, Basic Science Domain, Baker Heart and Diabetes Institute, Melbourne, VIC, Australia.
Baker Heart and Diabetes Institute · AUThe University of Melbourne · AUWestmead Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is now increasingly appreciated that inflammation is not limited to the control of pathogens by the host, but rather that sterile inflammation which occurs in the absence of viral or bacterial pathogens, accompanies numerous disease states, none more so than the complications that arise as a result of hyperglycaemia. Individuals with type 1 or type 2 diabetes mellitus (T1D, T2D) are at increased risk of developing cardiac and vascular complications. Glucose and blood pressure lowering therapies have not stopped the advance of these morbidities that often lead to fatal heart attacks and/or stroke. A unifying mechanism of hyperglycemia-induced cellular damage was initially proposed to link elevated blood glucose levels with oxidative stress and the dysregulation of metabolic pathways. Pre-clinical evidence has, in most cases, supported this notion. However, therapeutic strategies to lessen oxidative stress in clinical trials has not proved efficacious, most likely due to indiscriminate targeting by antioxidants such as vitamins. Recent evidence now suggests that oxidative stress is a major driver of inflammation and vice versa, with the latest findings suggesting not only a key role for inflammatory pathways underpinning metabolic and haemodynamic dysfunction in diabetes, but furthermore that these perturbations are driven by activation of the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome. This review will address these latest findings with an aim of highlighting the interconnectivity between oxidative stress, NLRP3 activation and inflammation as it pertains to cardiac and vascular injury sustained by diabetes. Current therapeutic strategies to lessen both oxidative stress and inflammation will be emphasized. This will be placed in the context of improving the burden of these diabetic complications.

Indexed as

diabetic atherosclerosisdiabetic cardiomyopathydiabetic complicationsdiabetic nephropathyinflammationinflammatory cytokinesNLRP3 inflammasomeoxidative stress

Identifiers

PMID29515457
PMCPMC5826188
OpenAlexW2794169913

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.