ArticleScientific reports2017
Silencing salusin-β attenuates cardiovascular remodeling and hypertension in spontaneously hypertensive rats.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- METTL3 mediates mJournal of advanced research · 2026Article
- Salusin-β, Arterial Stiffness, and Heart Rate Variability Influence the Blood Pressure Response to High-Intensity Interval Training Among Older Adults With Hypertension: A Randomized Control Trial.Health science reports · 2025Article
- Oxidative Stress Biomarkers in Hypertension.Current medicinal chemistry · 2025Review
- Downregulation of salusins alleviates hypertrophic cardiomyopathy via attenuating oxidative stress and autophagy.European journal of medical research · 2024Article
- The Clinical Significance of Salusins in Systemic Sclerosis-A Cross-Sectional Study.Diagnostics (Basel, Switzerland) · 2023Article
- Salusin-β, a TOR2A gene product, promotes proliferation, migration, fibrosis, and calcification of smooth muscle cells and accelerates the imbalance of vasomotor function and vascular remodeling in monocrotaline-induced pulmonary hypertensive rats.Frontiers in pharmacology · 2022Article
- Salusin-β in Intermediate Dorsal Motor Nucleus of the Vagus Regulates Sympathetic-Parasympathetic Balance and Blood Pressure.Biomedicines · 2021Article
- A TOR2A Gene Product: Salusin-β Contributes to Attenuated Vasodilatation of Spontaneously Hypertensive Rats.Cardiovascular drugs and therapy · 2021Article
- 3D-printed cranial models simulating operative field depth for microvascular training in neurosurgery.Surgical neurology international · 2021Article
- TLR4 regulates vascular smooth muscle cell proliferation in hypertension via modulation of the NLRP3 inflammasome.American journal of translational research · 2021Article
- Improvement of Vascular Function by Knockdown of Salusin-β in Hypertensive Rats via Nitric Oxide and Reactive Oxygen Species Signaling Pathway.Frontiers in physiology · 2021Article
- Knockdown of Salusin-Oxidative medicine and cellular longevity · 2021Article
- Salusin-β mediates tubular cell apoptosis in acute kidney injury: Involvement of the PKC/ROS signaling pathway.Redox biology · 2020Article
- Collagen receptor cross-talk determines α-smooth muscle actin-dependent collagen gene expression in angiotensin II-stimulated cardiac fibroblasts.The Journal of biological chemistry · 2019Article
- Salusin-β Promotes Vascular CalcificationAntioxidants & redox signaling · 2019Article
- Article
- BCL6 Attenuates Proliferation and Oxidative Stress of Vascular Smooth Muscle Cells in Hypertension.Oxidative medicine and cellular longevity · 2019Article
- Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Salusin-β is a bioactive peptide involved in vascular smooth muscle cell proliferation, vascular fibrosis and hypertension. The present study was designed to determine the effects of silencing salusin-β on hypertension and cardiovascular remodeling in spontaneously hypertensive rats (SHR). Thirteen-week-old male SHR and normotensive Wistar-Kyoto rats (WKY) were subjected to intravenous injection of PBS, adenoviral vectors encoding salusin-β shRNA (Ad-Sal-shRNA) or a scramble shRNA. Salusin-β levels in plasma, myocardium and mesenteric artery were increased in SHR. Silencing salusin-β had no significant effect on blood pressure in WKY, but reduced blood pressure in SHR. It reduced the ratio of left ventricle weight to body weight, cross-sectional areas of cardiocytes and perivascular fibrosis, and decreased the media thickness and the media/lumen ratio of arteries in SHR. Silencing salusin-β almost normalized plasma norepinephrine and angiotensin II levels in SHR. It prevented the upregulation of angiotensin II and AT
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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.