Evidence map›Paper›PMID 24665124›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2014

2013 Russell Ross memorial lecture in vascular biology: cellular and molecular mechanisms of diabetes mellitus-accelerated atherosclerosis.

Karin E Bornfeldt

Open access · bronzeAbstract readLecture
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
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  3. [Progress of pathogenesis and genetics of alcohol-induced osteonecrosis of femoral head].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2022
    Review
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  19. Morphometric and histological parameters in veins of diabetic patients undergoing brachiocephalic fistula placement.Hemodialysis international. International Symposium on Home Hemodialysis · 2015
    Article
  20. Article
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

1 author at 1 institution in 2 countries.

Karin E BornfeldtFrom the Department of Medicine, Division of Metabolism, Endocrinology and Nutrition, and Department of Pathology, Diabetes and Obesity Center of Excellence, University of Washington, Seattle, WA.
University of Washington · US

Funding

Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Karin E Bornfeldt · 1986 to 2026
$41.4M
Role of Serum Amyloid A in Diabetic Vascular DiseaseP01HL092969 · NHLBI · UNIVERSITY OF WASHINGTON · PI BORNFELDT, KARIN E. · 2008 to 2019
$23.5M
HYPERGLYCEMIA, PROTEIN KINASES AND SMOOTH MUSCLE GROWTHR01HL062887 · NHLBI · UNIVERSITY OF WASHINGTON · PI BORNFELDT, KARIN E. · 1998 to 2014
$4.7M
S100A9 and S100A8 in Diabetes and AtherosclerosisR01HL097365 · NHLBI · UNIVERSITY OF WASHINGTON · PI BORNFELDT, KARIN E. · 2010 to 2013
$1.6M
British Heart FoundationNHLBI NIH HHS P01 HL092969NHLBI NIH HHS P01HL092969NHLBI NIH HHS R01 HL062887NHLBI NIH HHS R01HL062887NHLBI NIH HHS R01 HL097365NHLBI NIH HHS R01HL097365NIDDK NIH HHS P30 DK017047NIDDK NIH HHS P30DK017047
6 · The paper itself

Abstract

Adults with diabetes mellitus are much more likely to have cardiovascular disease than those without diabetes mellitus. Genetically engineered mouse models have started to provide important insight into the mechanisms whereby diabetes mellitus promotes atherosclerosis. Such models have demonstrated that diabetes mellitus promotes formation of atherosclerotic lesions, progression of lesions into advanced hemorrhaged lesions, and that it prevents lesion regression. The proatherosclerotic effects of diabetes mellitus are driven in part by the altered function of myeloid cells. The protein S100A9 and the receptor for advanced glycation end-products are important modulators of the effect of diabetes mellitus on myelopoiesis, which might promote monocyte accumulation in lesions. Furthermore, myeloid cell expression of the enzyme acyl-CoA synthetase 1 (ACSL1), which converts long-chain fatty acids into their acyl-CoA derivatives, has emerged as causal to diabetes mellitus-induced lesion initiation. The protective effects of myeloid ACSL1-deficiency in diabetic mice, but not in nondiabetic mice, indicate that myeloid cells are activated by diabetes mellitus through mechanisms that play minor roles in the absence of diabetes mellitus. The roles of reactive oxygen species and insulin resistance in diabetes mellitus-accelerated atherosclerosis are also discussed, primarily in relation to endothelial cells. Translational studies addressing whether the mechanisms identified in mouse models are equally important in humans with diabetes mellitus will be paramount.

Indexed as

Signal TransductionAnimalsAtherosclerosisBlood GlucoseBlood VesselsDiabetic AngiopathiesDisease Models, AnimalDisease ProgressionGenetic Predisposition to DiseaseHumansInsulin ResistanceMiceMice, TransgenicPhenotypeRisk FactorsTime FactorsBlood Glucoseatherosclerosisdiabetes mellitusendothelial cellsmacrophagesmice

Identifiers

PMID24665124
PMCPMC3967130
OpenAlexW2586950898

What OpenQuestion holds

Textmetadata
LicenceTDM
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.