Evidence map›Paper›PMID 27353274›Full record

ArticleHistology and histopathology2017

Histopathological assessment of calcification and inflammation of calcific aortic valves from patients with and without diabetes mellitus.

Josephin Mosch, Christian A Gleissner, Simon Body, Elena Aikawa

Abstract read
In one paragraph

Article in Histology and histopathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.1field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

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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

31 citing papers in PubMed, 46 citations in OpenAlex.

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  20. Aortic valve disease in diabetes: Molecular mechanisms and novel therapies.Journal of cellular and molecular medicine · 2021
    Review
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

4 authors at 3 institutions in 2 countries.

Josephin MoschCenter of Excellence in Vascular Biology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, USA.
Christian A GleissnerDepartment of Cardiology, University Hospital, Heidelberg, Germany.
Simon BodyDepartment of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, USA.
Elena AikawaCenter of Excellence in Vascular Biology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, USA.
Harvard University · USHeidelberg University · DEUniversity Hospital Heidelberg · DE

Funding

Improving Mitral Compensation in Ischemic RegurgitationR01HL109506 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI AIKAWA, ELENA, BISCHOFF, JOYCE E. · 2012 to 2015
$3.3M
Macrophage-derived microcalcificaitonsR01HL136431 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI AIKAWA, ELENA · 2017 to 2020
$2.7M
Genetic Etiology of Bicuspid Aortic Valve DiseaseR01HL114823 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI BODY, SIMON C · 2012 to 2016
$2.1M
Aortic valve microcalcificationR01HL114805 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI AIKAWA, ELENA · 2012 to 2016
$2.1M
NHLBI NIH HHS R01 HL109506NHLBI NIH HHS R01 HL114805NHLBI NIH HHS R01 HL114823NHLBI NIH HHS R01 HL136431
6 · The paper itself

Abstract

backgroundCalcific aortic valve disease (CAVD) is the most common valvular heart disease and likely evolves from inflammatory pre-conditions in the valve. Type II diabetes mellitus (DMII) has been associated with pathogenesis of CAVD, however, the mechanism initiating CAVD in DMII is not well understood and the human valve pathology in DMII has not been described. We therefore performed quantitative histological analyses of aortic valves of CAVD patients with and without DMII.

methodsCAVD human aortic valves (n=45) obtained after surgical valve replacement were examined macroscopically with gross measurements of calcified areas. Inflammation and calcification were assessed by immunohistochemistry and immunofluorescence staining.

resultsCalcification was increased in diabetic patients according to gross measurements (p<0.01) and alizarin red staining (p=0.05). Early calcification markers, including Runx2 (p=0.02) and alkaline phosphatase (ALP, p=0.03) were significantly elevated in diabetic patients. Furthermore, in diabetic patients we found significantly increased expression of annexin II (p=0.04) and annexin V (p=0.04), both of which are thought to play a role in microcalcification formation via apoptosis or extracellular vesicle release. Macrophage numbers were comparable in both groups (p=0.41), while the expression of the pro-inflammatory protein S100A9 (p<0.01) was significantly decreased in diabetic individuals. Evaluation of lymphocytes revealed similar CD8 (p=0.45) and CD4 (p=0.92) T cell counts in diabetic and non-diabetic aortic valves.

conclusionAortic valves from diabetic patients show more calcification, while inflammation is similar in both patient populations. Considering the generally accepted theory of an inflammation-dependent mechanism of calcification, these data suggest that in patients with CAVD requiring valve replacement, diabetic patients could be molecularly in a more advanced disease stage with a higher grade of mineralization than non-diabetic patients.

Indexed as

AgedAortic ValveAortic Valve StenosisCalcinosisDiabetes Mellitus, Type 2FemaleHumansInflammationMaleMiddle Aged

Identifiers

PMID27353274
PMCPMC5199639
OpenAlexW2475690432

What OpenQuestion holds

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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.