ArticleJournal of translational medicine2018
Endoplasmic reticulum stress in perivascular adipose tissue promotes destabilization of atherosclerotic plaque by regulating GM-CSF paracrine.
Article in Journal of translational medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Impact of Cardiovascular Diseases on COVID-19: A Systematic Review.Medical science monitor : international medical journal of experimental and clinical research · 2021Pooled it
- CL-316243 facilitates stable atherosclerotic plaque phenotypes in association with suppression of perivascular adipose tissue ferroptosis via upregulating C/EBPβ.Redox biology · 2026Article
- Cell-Penetrating Peptide-Mediated Modulation of Endoplasmic Reticulum Stress: A Bioengineered and Translational Approach.ACS pharmacology & translational science · 2026Review
- Exercise reverses high-fat diet-induced perivascular adipose tissue dysfunction through modulation of UCP2 and TXNIP/NLRP3 pathways.Journal of physiology and biochemistry · 2026Article
- VEGF-B is a novel mediator of ER stress which induces cardiac angiogenesis via RGD-binding integrins independent of VEGFR1/NRP activities.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Perivascular adipose tissue: a central player in the triad of diabetes, obesity, and cardiovascular health.Cardiovascular diabetology · 2024Review
- Endoplasmic reticulum stress: a novel targeted approach to repair bone defects by regulating osteogenesis and angiogenesis.Journal of translational medicine · 2023Review
- Role of GM-CSF in lung balance and disease.Frontiers in immunology · 2023Review
- Insights by which TUDCA is a potential therapy against adiposity.Frontiers in endocrinology · 2023Review
- Exploring the Relationship of Perivascular Adipose Tissue Inflammation and the Development of Vascular Pathologies.Mediators of inflammation · 2022Review
- Roles of Perivascular Adipose Tissue in Hypertension and Atherosclerosis.Antioxidants & redox signaling · 2021Review
- PVAT: an important guardian of the cardiovascular system.Histology and histopathology · 2020Review
- ER stress activates immunosuppressive network: implications for aging and Alzheimer's disease.Journal of molecular medicine (Berlin, Germany) · 2020Review
- Potential role of perivascular adipose tissue in modulating atherosclerosis.Clinical science (London, England : 1979) · 2020Review
- Perivascular Adipose Tissue as an Indication, Contributor to, and Therapeutic Target for Atherosclerosis.Frontiers in physiology · 2020Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundPerivascular adipose tissue (PVAT) accelerates plaque progression and increases cardiovascular risk. We tested the hypothesis that PVAT contributed to plaque vulnerability and investigated whether endoplasmic reticulum stress (ER stress) in PVAT played an important role in vulnerable plaque.
methodsWe transplanted thoracic aortic PVAT or subcutaneous adipose tissue as a control, from donor mice to carotid arteries of recipient apolipoprotein E deficient (apoE
resultsUltrastructural detection by transmission electron microscopy showed transplanted PVAT was a mixed population of white and brown adipocytes with abundant mitochondria. Transplanted PVAT increased the intraplaque macrophage infiltration, lipid core, intimal and vasa vasorum neovascularization and MMP2/9 expression in plaque while decreased smooth muscle cells and collagen in atherosclerotic plaque, which were restored by local 4-PBA-treatment. Antibody array analysis showed that 4-PBA reduced several angiogenic factors [Granulocyte Macrophage Colony Stimulating Factor (GM-CSF), MCP-1, IL-6] secreted by PVAT. Besides, conditioned medium from 4-PBA treated-PVAT inhibited tube formation and migration capacity of endothelial cells and ex vivo mouse aortic ring angiogenesis compared to conditioned medium from transplanted PVAT. mRNA expression and protein levels of GM-CSF were markedly elevated in adipocytes under ER stress which would be suppressed by 4-PBA. In addition, ER stress enhanced NF-κB binding to the promoter of the mouse GM-CSF gene in adipocytes confirmed by Chromatin immunoprecipitation analyses.
conclusionsOur findings demonstrate that ER stress in PVAT destabilizes atherosclerotic plaque, in part through increasing GM-CSF paracrine via transcription factor NF-κB.
Indexed as
Identifiers
What Socratic holds
Registered trials
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 Socratic graph.