ReviewMedGenMed : Medscape general medicine2004
Advances in diabetes for the millennium: diabetes and the endothelium.
Review in MedGenMed : Medscape general medicine, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed, 19 citations in OpenAlex.
- Platelet hemostasis in patients with metabolic syndrome and type 2 diabetes mellitus: cGMP- and NO-dependent mechanisms in the insulin-mediated platelet aggregation.Frontiers in physiology · 2014Review
- The prostacyclin analog beraprost sodium ameliorates characteristics of metabolic syndrome in obese Zucker (fatty) rats.Diabetes · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The normal endothelium performs the function of vasodilation, platelet inhibition, and the suppression of inflammation through the secretion of nitric oxide (NO) and prostacyclin (PGI2). Endothelial damage through diabetes, hypercholesterolemia, and other atherosclerotic risk factors results in the reduction of NO and PGI2 synthesis and secretion; and these changes turn the blood vessel into a proconstrictor, proaggregatory, and proinflammatory state. Because atherosclerosis is a chronic inflammation of the arterial wall, abnormal endothelial function would predispose the artery to atherogenesis and to a prothrombotic state. Recent studies have demonstrated that insulin exerts an anti-inflammatory effect in addition to inhibiting platelet aggregation and the expression of other prothrombotic factors. These facts challenge the conventional view that insulin is the mediator of atherogenesis in insulin-resistant states of obesity and type 2 diabetes, which are characterized by hyperinsulinemia. Furthermore, insulin has been shown to be anti-inflammatory, antioxidant, and profibrinolytic and cardioprotective in patients with acute myocardial infarction. Insulin is required as an anti-inflammatory hormone with potential antiatherosclerotic effects.
Indexed as
Identifiers
15647711PMC1474826W3149700216What OpenQuestion holds
Registered trials
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.