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Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues
Published on: June 3, 2019
Qsox1 Contributes to Vascular Remodelling in Response to Hypertension
Malha Sadoune1, Jérome Mourad1, Céline Luc1
1INSERM UMR-S 942 and Paris University, Paris, France.
Vascular sulfhydryl oxidase (QSOX1) is crucial for adaptive arterial remodeling in hypertension. Loss of QSOX1 impairs vascular smooth muscle cell adaptation, leading to heart failure and fibrosis under pressure overload.
Area of Science:
- Cardiovascular Research
- Biochemistry
- Hypertension Pathophysiology
Background:
- QSOX1 (sulfhydryl oxidase) is implicated in arterial remodeling.
- QSOX1 is a potential biomarker for preeclampsia and acute heart failure.
- The cardiovascular roles of QSOX1 in hypertension remain to be fully elucidated.
Purpose of the Study:
- To investigate the cardiovascular functions of QSOX1.
- To determine the role of QSOX1 in angiotensin II-induced hypertension.
- To understand QSOX1's contribution to vascular smooth muscle cell adaptation.
Main Methods:
- Utilized Qsox1-invalidated (Qsox1-/-) mice and VSMC-specific Qsox1 knockout models.
- Induced hypertension using angiotensin II infusion and Trans-Aortic Constriction (TAC).
- Assessed cardiac function, vessel morphology, and VSMC phenotype.
Main Results:
- Qsox1-/- mice exhibited lower baseline blood pressure and immature VSMC phenotype.
- Angiotensin II infusion in Qsox1-/- mice led to acute heart failure, absent coronary media hypertrophy, and increased fibrosis.
- VSMC-specific Qsox1 knockout impaired VSMC phenotype but did not affect cardiac function under AngII-induced hypertension.
Conclusions:
- Vascular QSOX1 plays a critical role in adaptive VSMC responses to pressure overload.
- QSOX1 is essential for the development of media hypertrophy in response to hypertension.
- These findings highlight QSOX1 as a key mediator in cardiovascular adaptation to hypertensive stress.
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