Evidence map›Paper›PMID 24687627›Full record

ReviewJournal of molecular medicine (Berlin, Germany)2014

The pathobiology of diabetic vascular complications--cardiovascular and kidney disease.

Stephen P Gray, Karin Jandeleit-Dahm

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of molecular medicine (Berlin, Germany), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 2 pooled it
4.8field-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

43 citing papers in PubMed, 2 syntheses or guidelines pooled it, 80 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

2 authors at 1 institution in 1 country.

Stephen P GrayDiabetes Complications Division, Baker IDI Heart & Diabetes Research Institute, PO Box 6492, St Kilda Rd, Melbourne, VIC, 8008, Australia, Stephen.gray@bakeridi.edu.au.
Karin Jandeleit-Dahm
Baker Heart and Diabetes Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

With the increasing incidence of obesity and type 2 diabetes, it is predicted that more than half of Americans will have diabetes or pre-diabetes by 2020. Diabetic patients develop vascular complications at a much faster rate in comparison to non-diabetic individuals, and cardiovascular risk is increased up to tenfold. With the increasing incidence of diabetes across the world, the development of vascular complications will become an increasing medical burden. Diabetic vascular complications affect the micro- and macro-vasculature leading to kidney disease often requiring dialysis and transplantation or cardiovascular disease increasing the risk for myocardial infarction, stroke and amputations as well as leading to premature mortality. It has been suggested that many complex pathways contribute to the pathobiology of diabetic complications including hyperglycaemia itself, the production of advanced glycation end products (AGEs) and interaction with the receptors for AGEs such as the receptor for advanced glycation end products (RAGE), as well as the activation of vasoactive systems such as the renin-angiotensin aldosterone system (RAAS) and the endothelin system. More recently, it has been hypothesised that reactive oxygen species derived from NAD(P)H oxidases (Nox) may represent a common downstream mediator of vascular injury in diabetes. Current standard treatment of care includes the optimization of blood glucose and blood pressure usually including inhibitors of the renin-angiotensin system. Although these interventions are able to delay progression, they fail to prevent the development of complications. Thus, there is an urgent medical need to identify novel targets in diabetic vascular complications which may include the blockade of Nox-derived ROS formation, as well as blockade of AGE formation and inhibitors of RAGE activation. These strategies may provide superior protection against the deleterious effects of diabetes on the vasculature.

Indexed as

AnimalsCardiovascular DiseasesDiabetes Mellitus, Type 2Diabetic AngiopathiesGlycation End Products, AdvancedHumansKidney DiseasesNADPH OxidasesOxidative StressReactive Oxygen SpeciesRenin-Angiotensin SystemGlycation End Products, AdvancedNADPH OxidasesReactive Oxygen Species

Identifiers

PMID24687627
OpenAlexW2053451373

What OpenQuestion holds

Textmetadata
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.