Evidence map›Paper›PMID 23449456›Full record

ArticleCell death & disease2013

Role of protein kinase C δ in ER stress and apoptosis induced by oxidized LDL in human vascular smooth muscle cells.

P Larroque-Cardoso, A Swiader, C Ingueneau, A Nègre-Salvayre, M Elbaz, M E Reyland, R Salvayre, C Vindis

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

47 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Review
  3. Emerging role of IRE1α in vascular diseases.Journal of cell communication and signaling · 2024
    Review
  4. Review
  5. PKCδ regulates the vascular biology in diabetic atherosclerosis.Cell communication and signaling : CCS · 2023
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Senescence in Vascular Smooth Muscle Cells and Atherosclerosis.Frontiers in cardiovascular medicine · 2022
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  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

8 authors at 2 institutions in 2 countries.

P Larroque-CardosoINSERM UMR 1048/I2MC, Toulouse, France.
A Swiader
C Ingueneau
A Nègre-Salvayre
M Elbaz
M E Reyland
R Salvayre
C Vindis
Inserm · FRUniversity of Colorado Denver · US

Funding

Regulation of Salivary Cell Apoptosis by Protein Kinase CR01DE015648 · NIDCR · UNIVERSITY OF COLORADO DENVER · PI REYLAND, MARY ELAINE · 2004 to 2019
$5.6M
6 · The paper itself

Abstract

During atherogenesis, excess amounts of low-density lipoproteins (LDL) accumulate in the subendothelial space where they undergo oxidative modifications. Oxidized LDL (oxLDL) alter the fragile balance between survival and death of vascular smooth muscle cells (VSMC) thereby leading to plaque instability and finally to atherothrombotic events. As protein kinase C δ (PKCδ) is pro-apoptotic in many cell types, we investigated its potential role in the regulation of VSMC apoptosis induced by oxLDL. We found that human VSMC silenced for PKCδ exhibited a protection towards oxLDL-induced apoptosis. OxLDL triggered the activation of PKCδ as shown by its phosphorylation and nuclear translocation. PKCδ activation was dependent on the reactive oxygen species generated by oxLDL. Moreover, we demonstrated that PKCδ participates in oxLDL-induced endoplasmic reticulum (ER) stress-dependent apoptotic signaling mainly through the IRE1α/JNK pathway. Finally, the role of PKCδ in the development of atherosclerosis was supported by immunohistological analyses showing the colocalization of activated PKCδ with ER stress and lipid peroxidation markers in human atherosclerotic lesions. These findings highlight a role for PKCδ as a key regulator of oxLDL-induced ER stress-mediated apoptosis in VSMC, which may contribute to atherosclerotic plaque instability and rupture.

Indexed as

ApoptosisEndoplasmic Reticulum StressAnimalsCell NucleusCells, CulturedEndoribonucleasesHumansJNK Mitogen-Activated Protein KinasesLipoproteins, LDLMiceMuscle, Smooth, VascularPhosphorylationProtein Kinase C-deltaProtein Serine-Threonine KinasesReactive Oxygen SpeciesRNA InterferenceEndoribonucleasesERN1 protein, humanJNK Mitogen-Activated Protein KinasesLipoproteins, LDLoxidized low density lipoproteinProtein Kinase C-deltaProtein Serine-Threonine KinasesReactive Oxygen SpeciesRNA, Small Interfering

Identifiers

PMID23449456
PMCPMC3734829
OpenAlexW2083107204

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.