Evidence map›Paper›PMID 32118048›Full record

ReviewFrontiers in cardiovascular medicine2020

Monocytes and Macrophages as Protagonists in Vascular Complications of Diabetes.

Jenny E Kanter, Cheng-Chieh Hsu, Karin E Bornfeldt

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cardiovascular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
7.7field-weighted citation impact, top 2% 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

59 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.

  1. Pooled it
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  19. Therapeutic potential ofOpen veterinary journal · 2024
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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

3 authors at 1 institution in 1 country.

Jenny E KanterDepartment of Medicine, University of Washington Medicine Diabetes Institute, University of Washington School of Medicine, Seattle, WA, United States.
Cheng-Chieh HsuDepartment of Medicine, University of Washington Medicine Diabetes Institute, University of Washington School of Medicine, Seattle, WA, United States.
Karin E BornfeldtDepartment of Medicine, University of Washington Medicine Diabetes Institute, University of Washington School of Medicine, Seattle, WA, United States.
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
Proteolytic control of local inflammatory macrophage proliferationR01HL127694 · NHLBI · UNIVERSITY OF WASHINGTON · PI BORNFELDT, KARIN E. · 2015 to 2018
$2.0M
Probing human leukocytes to target inflammatory macrophage proliferation in chronic inflammationR21AI135447 · NIAID · UNIVERSITY OF WASHINGTON · PI BORNFELDT, KARIN E. · 2018 to 2019
$427k
NHLBI NIH HHS P01 HL092969NHLBI NIH HHS R01 HL127694NIAID NIH HHS R21 AI135447NIDDK NIH HHS P30 DK017047
6 · The paper itself

Abstract

With the increasing prevalence of diabetes worldwide, vascular complications of diabetes are also on the rise. Diabetes results in an increased risk of macrovascular complications, with atherosclerotic cardiovascular disease (CVD) being the leading cause of death in adults with diabetes. The exact mechanisms for how diabetes promotes CVD risk are still unclear, although it is evident that monocytes and macrophages are key players in all stages of atherosclerosis both in the absence and presence of diabetes, and that phenotypes of these cells are altered by the diabetic environment. Evidence suggests that at least five pro-atherogenic mechanisms involving monocytes and macrophages contribute to the accelerated atherosclerotic lesion progression and hampered lesion regression associated with diabetes. These changes include (1) increased monocyte recruitment to lesions; (2) increased inflammatory activation; (3) altered macrophage lipid accumulation and metabolism; (4) increased macrophage cell death; and (5) reduced efferocytosis. Monocyte and macrophage phenotypes and mechanisms have been revealed mostly by different animal models of diabetes. The roles of specific changes in monocytes and macrophages in humans with diabetes remain largely unknown. There is an ongoing debate on whether the changes in monocytes and macrophages are caused by altered glucose levels, insulin deficiency or insulin resistance, lipid abnormalities, or combinations of these factors. Current research in humans and mouse models suggests that reduced clearance of triglyceride-rich lipoproteins and their remnants is one important mechanism whereby diabetes adversely affects macrophages and promotes atherosclerosis and CVD risk. Although monocytes and macrophages readily respond to the diabetic environment and can be seen as protagonists in diabetes-accelerated atherosclerosis, they are likely not instigators of the increased CVD risk.

Indexed as

apolipoprotein C3atherosclerosiscytokinesdiabetesefferocytosismonocytosisnecrotic core

Identifiers

PMID32118048
PMCPMC7033616
OpenAlexW3006312449

What OpenQuestion holds

Textmetadata
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.