ArticlePloS one2014
Salusin-β not salusin-α promotes vascular inflammation in ApoE-deficient mice via the I-κBα/NF-κB pathway.
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 14 papers.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- Article
- The Clinical Significance of Salusins in Systemic Sclerosis-A Cross-Sectional Study.Diagnostics (Basel, Switzerland) · 2023Article
- Serum salusin-α and salusin-β levels in patients with psoriatic arthritis.Reumatologia · 2022Article
- Anti‑inflammatory effect of salusin‑β knockdown on LPS‑activated alveolar macrophages via NF‑κB inhibition and HO‑1 activation.Molecular medicine reports · 2021Article
- Salusin-The Journal of international medical research · 2020Article
- Taoren Honghua Drug Attenuates Atherosclerosis and Plays an Anti-Inflammatory Role in ApoE Knock-Out Mice and RAW264.7 Cells.Frontiers in pharmacology · 2020Article
- Relationship of serum salusin beta levels with coronary slow flow.Anatolian journal of cardiology · 2019Article
- Relationship of salusin-alpha and salusin-beta levels with atherosclerosis in patients undergoing haemodialysis.Singapore medical journal · 2019Article
- Overexpression of Salusin-BioMed research international · 2018Article
- Salusin-Oxidative medicine and cellular longevity · 2017Article
- Is the serum level of salusin-β associated with hypertension and atherosclerosis in the pediatric population?Pediatric nephrology (Berlin, Germany) · 2015Article
- Salusin-β, but not salusin-α, promotes human umbilical vein endothelial cell inflammation via the p38 MAPK/JNK-NF-κB pathway.PloS one · 2014Article
- Anti-atherogenic effect of hydrogen sulfide by over-expression of cystathionine gamma-lyase (CSE) gene.PloS one · 2014Article
- Prognostic Value of Serum Salusin-α and Salusin-β in COVID-19 Patients.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/HemostasisArticle
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveVascular inflammation plays an important role in the development and progression of atherosclerosis. Recently, salusins (salusin-α and salusin-β) have been reported to be associated wtih atherosclerosis. However, its underlying mechanism remains incompletely known. In this study, we observed the effects of salusins on vascular inflammation in apoE-deficient (apoE-/-) mice. METHODS AND
resultsSix-week old male apoE-/- mice were infused with salusin-α, salusin-β or vehicle for 8 weeks via osmotic mini-pumps. Our results showed that apoE-/- mice receiving vehicle alone developed severe atherosclerotic lesions and dyslipidemia, with significantly up-regulated levels of IL-6, TNF-α, VCAM-1 and MCP-1. For apoE-/- mice receiving 8 weeks of salusin-β infusion, the atherosclerotic lesions were markedly aggravated, and the levels of IL-6, TNF-α, VCAM-1 and MCP-1 were substantially increased, despite a similar plasma lipid concentration with that of apoE-/- mice. However, after 8 week-infusion of salusin-α, apoE-/- mice presented significant amelioration in atherosclerotic lesions, along with remarkably up-regulated level of high-density lipoprotein-cholesterol (HDL-C) and down-regulated levels of IL-6 and TNF-α, but without any effect on the expressions of VCAM-1 and MCP-1. Furthermore, the activation of nuclear factor-κB (NF-κB), an important transcription factor essential for inflammatory molecules, and the degradation of I-κBα, an inhibitor of NF-κB, were markedly increased in apoE-/- mice receiving vehicle alone. Treatment with salusin-β not salusin-α could remarkably accelerate the process of NF-κB nuclear translocation and I-κBα degradation.
conclusionSalusin-β, but not salusin-α, promotes vascular inflammation in apoE-deficient mice via the I-κBα/NF-κB pathway. These findings provide further insight into the mechanism of salusins in atherosclerosis and potential targets for the prevention and treatment of atherosclerosis.
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