Evidence map›Paper›PMID 22879584›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2012

Elevated protein kinase C-δ contributes to aneurysm pathogenesis through stimulation of apoptosis and inflammatory signaling.

Stephanie Morgan, Dai Yamanouchi, Calvin Harberg, Qiwei Wang, Melissa Keller, Yi Si, William Burlingham, Stephen Seedial, Justin Lengfeld, Bo Liu

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

33 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. IRF8 Drives Conventional Type 1 Dendritic Cell Differentiation and CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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  3. RAGE deficiency ameliorates abdominal aortic aneurysm progression.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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  10. Platelet-Activating Factor Promotes the Development of Non-Alcoholic Fatty Liver Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022
    Review
  11. Identification ofFrontiers in cardiovascular medicine · 2022
    Article
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  15. Pathogenic mechanisms and the potential of drug therapies for aortic aneurysm.American journal of physiology. Heart and circulatory physiology · 2020
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Aortic Aneurysms.Arteriosclerosis, thrombosis, and vascular biology · 2017
    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

10 authors at 1 institution in 1 country.

Stephanie MorganDivision of Vascular Surgery, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA.
Dai Yamanouchi
Calvin Harberg
Qiwei Wang
Melissa Keller
Yi Si
William Burlingham
Stephen Seedial
Justin Lengfeld
Bo Liu
University of Wisconsin–Madison · US

Funding

Training Program in Translational Cardiovascular Science (TPTCS)T32HL007936 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI Lee Lochbaum Eckhardt, Gail A Robertson · 2001 to 2026
$11.6M
Molecular Mechanisms in Abdominal Aortic AneuysmR01HL088447 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI LIU, BO · 2011 to 2020
$3.8M
Howard Hughes Medical Institute MSN135276NHLBI NIH HHS R01 HL088447NHLBI NIH HHS R01HL088447NHLBI NIH HHS T32 HL007936NHLBI NIH HHS T32 HL 07936
6 · The paper itself

Abstract

objectiveApoptosis of smooth muscle cells (SMCs) is a prominent pathological characteristic of abdominal aortic aneurysm (AAA). We have previously shown that SMC apoptosis stimulates proinflammatory signaling in a mouse model of AAA. Here, we test whether protein kinase C-δ (PKCδ), an apoptotic mediator, participates in the pathogenesis of AAA by regulating apoptosis and proinflammatory signals. METHODS AND

resultsMouse experimental AAA is induced by perivascular administration of CaCl(2). Mice deficient in PKCδ exhibit a profound reduction in aneurysmal expansion, SMC apoptosis, and transmural inflammation as compared with wild-type littermates. Delivery of PKCδ to the aortic wall of PKCδ(-/-) mice restores aneurysm, whereas overexpression of a dominant negative PKCδ mutant in the aorta of wild-type mice attenuates aneurysm. In vitro, PKCδ(-/-) aortic SMCs exhibit significantly impaired monocyte chemoattractant protein-1 production. Ectopic administration of recombinant monocyte chemoattractant protein-1 to the arterial wall of PKCδ(-/-) mice restores inflammatory response and aneurysm development.

conclusionsPKCδ is an important signaling mediator for SMC apoptosis and inflammation in a mouse model of AAA. By stimulating monocyte chemoattractant protein-1 expression in aortic SMCs, upregulated PKCδ exacerbates the inflammatory process, in turn perpetuating elastin degradation and aneurysmal dilatation. Inhibition of PKCδ may serve as a potential therapeutic strategy for AAA.

Indexed as

Up-RegulationAnimalsAortic Aneurysm, AbdominalApoptosisCalcium ChlorideCell MovementCells, CulturedChemokine CCL2ElastinInflammationIn Vitro TechniquesMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutCalcium ChlorideCcl2 protein, mouseChemokine CCL2ElastinProtein Kinase C-delta

Identifiers

PMID22879584
PMCPMC3442600
OpenAlexW2132143276

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.