ArticlePloS one2014
Autophagic marker MAP1LC3B expression levels are associated with carotid atherosclerosis symptomatology.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed.
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- Antiatherogenic and Cardioprotective Effects of a Xanthine Derivative KMUP-1 in ApoE Knockout Mice.Cardiovascular therapeutics · 2025Article
- Cellular Senescence, Mitochondrial Dysfunction, and Their Link to Cardiovascular Disease.Cells · 2024Review
- Polymorphism of IL-12/IL-23 axis is associated with coronary heart disease.Journal of cellular and molecular medicine · 2024Article
- MiR-483-5p downregulation alleviates ox-LDL induced endothelial cell injury in atherosclerosis.BMC cardiovascular disorders · 2023Article
- Comprehensive analysis of autophagy-related gene expression profiles identified five gene biomarkers associated with immune infiltration and advanced plaques in carotid atherosclerosis.Orphanet journal of rare diseases · 2023Article
- Mitochondrial quality control in health and cardiovascular diseases.Frontiers in cell and developmental biology · 2023Review
- Mitochondrial autophagy: molecular mechanisms and implications for cardiovascular disease.Cell death & disease · 2022Review
- Identification of an autophagy-related gene signature for predicting prognosis and immune activity in pancreatic adenocarcinoma.Scientific reports · 2022Article
- miR-451-3p alleviates myocardial ischemia/reperfusion injury by inhibiting MAP1LC3B-mediated autophagy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Article
- Effects of Urolithin A on Mitochondrial Parameters in a Cellular Model of Early Alzheimer Disease.International journal of molecular sciences · 2021Article
- Autophagy-Related Genes in Atherosclerosis.Journal of healthcare engineering · 2021Article
- Autophagy, Pyroptosis, and Ferroptosis: New Regulatory Mechanisms for Atherosclerosis.Frontiers in cell and developmental biology · 2021Review
- Superoxide Dismutase 2 (SOD2) in Vascular Calcification: A Focus on Vascular Smooth Muscle Cells, Calcification Pathogenesis, and Therapeutic Strategies.Oxidative medicine and cellular longevity · 2021Review
- Article
- Review
- Mitochondrial Dysfunction and DNA Damage in the Context of Pathogenesis of Atherosclerosis.Biomedicines · 2020Review
- Mitophagy in Cardiovascular Diseases.Journal of clinical medicine · 2020Review
- Myeloid atg5 deletion impairs n-3 PUFA-mediated atheroprotection.Atherosclerosis · 2020Article
- Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesThe mechanism by which atheroma plaque becomes unstable is not completely understood to date but analysis of differentially expressed genes in stable versus unstable plaques may provide clues. This will be crucial toward disclosing the mechanistic basis of plaque instability, and may help to identify prognostic biomarkers for ischaemic events. The objective of our study was to identify differences in expression levels of 59 selected genes between symptomatic patients (unstable plaques) and asymptomatic patients (stable plaques).
methods80 carotid plaques obtained by carotid endarterectomy and classified as symptomatic (>70% stenosis) or asymptomatic (>80% stenosis) were used in this study. The expression levels of 59 genes were quantified by qPCR on RNA extracted from the carotid plaques obtained by endarterectomy and analyzed by means of various bioinformatic tools.
resultsSeveral genes associated with autophagy pathways displayed differential expression levels between asymptomatic and symptomatic (i.e. MAP1LC3B, RAB24, EVA1A). In particular, mRNA levels of MAP1LC3B, an autophagic marker, showed a 5-fold decrease in symptomatic samples, which was confirmed in protein blots. Immune system-related factors and endoplasmic reticulum-associated markers (i.e. ERP27, ITPR1, ERO1LB, TIMP1, IL12B) emerged as differently expressed genes between asymptomatic and symptomatic patients.
conclusionsCarotid atherosclerotic plaques in which MAP1LC3B is underexpressed would not be able to benefit from MAP1LC3B-associated autophagy. This may lead to accumulation of dead cells at lesion site with subsequent plaque destabilization leading to cerebrovascular events. Identified biomarkers and network interactions may represent novel targets for development of treatments against plaque destabilization and thus for the prevention of cerebrovascular events.
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