ArticleScientific reports2016
Protein Inhibitor of Activated STAT3 Suppresses Oxidized LDL-induced Cell Responses during Atherosclerosis in Apolipoprotein E-deficient Mice.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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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.
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Who cites it
33 citing papers in PubMed, 51 citations in OpenAlex.
- CircRNA0857 acts as an miRNA sponge to promote Newcastle disease virus replication via modulating autophagy.Journal of virology · 2026Article
- Andrographolide attenuates microglial senescence in Alzheimer's disease mice by suppressing the STAT3 signaling.iScience · 2026Article
- The asialoglycoprotein receptor 1 (ASGR1): emerging new roles in health and disease.Biomarker research · 2026Review
- Neutrophil-derived oncostatin m contributes to endothelial cell dysfunction during Treponema denticola interaction.PloS one · 2026Article
- The SIRT1/STAT3 axis as a central regulator of immune, inflammatory, and lipid metabolic dysregulation in rheumatoid arthritis: therapeutic implications.Frontiers in immunology · 2026Review
- The SGLT2 inhibitor empagliflozin attenuates atherosclerosis progression by inducing autophagy.Journal of physiology and biochemistry · 2024Article
- LncRNA/CircRNA-miRNA-mRNA Axis in Atherosclerotic Inflammation: Research Progress.Current pharmaceutical biotechnology · 2024Review
- Circular RNAs in vascular diseases.Frontiers in cardiovascular medicine · 2023Review
- Genetic deficiency of protein inhibitor of activated STAT3 suppresses experimental abdominal aortic aneurysms.Frontiers in cardiovascular medicine · 2023Article
- CircRNA-miRNA interactions in atherogenesis.Molecular and cellular biochemistry · 2022Review
- Upregulated miR-18a-5p in Colony Forming Unit-Hill's in Subclinical Cardiovascular Disease and Metformin Therapy; MERIT Study.Biomedicines · 2022Article
- MiR-130a-5p contributed to the progression of endothelial cell injury by regulating FAS.European journal of histochemistry : EJH · 2022Article
- The role of IL-6 in hyperlipidemia-induced accelerated rejection.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2022Article
- Circular RNAs as emerging regulators in COVID-19 pathogenesis and progression.Frontiers in immunology · 2022Review
- Vascular Protective Effect and Its Possible Mechanism of Action on Selected Active Phytocompounds: A Review.Evidence-based complementary and alternative medicine : eCAM · 2022Review
- Research methods for animal models of atherosclerosis (Review).Molecular medicine reports · 2021Article
- Novel HOpen medicine (Warsaw, Poland) · 2021Article
- Lysosome (Dys)function in Atherosclerosis-A Big Weight on the Shoulders of a Small Organelle.Frontiers in cell and developmental biology · 2021Review
- BTK Promotes Atherosclerosis by Regulating Oxidative Stress, Mitochondrial Injury, and ER Stress of Macrophages.Oxidative medicine and cellular longevity · 2021Article
- Punicalagin Attenuates Disturbed Flow-Induced Vascular Dysfunction by Inhibiting Force-Specific Activation of Smad1/5.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis is a serious public health concern. Excessive inflammatory responses of vascular cells are considered a pivotal pathogenesis mechanism underlying atherosclerosis development. It is known that Janus kinase/signal transducer and activator of transcription 3 (JAK/STAT3) signalling plays an important role in atherosclerosis progression. Protein inhibitor of activated STAT3 (PIAS3) is the key negative regulator of JAK/STAT3 signalling. However, its effect on atherogenesis is unknown. Here, we observed that PIAS3 levels are reduced in atherosclerotic lesions and that PIAS3 expression decreases in conjunction with increases in interleukin-6 expression and atherosclerosis severity. Oxidized low-density lipoprotein (ox-LDL), an atherogenic stimulus, reduced PIAS3 expression, an effect that may be attributed to nitric oxide synthesis upregulation. In turn, PIAS3 overexpression effectively suppressed ox-LDL-induced inflammation, lipid accumulation and vascular smooth muscle cell proliferation. These results indicate that PIAS3 is a critical repressor of atherosclerosis progression. The findings of this study have contributed to our understanding on the pathogenesis of atherosclerosis and have provided us with a potential target through which we can inhibit atherosclerosis-related cellular responses.
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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 OpenQuestion graph.