Asprosin as a Potential Link Between Vascular Inflammation and Disease Activity in Behcet's Disease
Küçük Resim Yok
Tarih
2026
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Wiley
Erişim Hakkı
info:eu-repo/semantics/openAccess
Özet
Objective: and design Mild vascular inflammation promotes the pathogenesis of hypertension. Asprosin, a newly discovered adipokine, is closely associated with metabolic diseases. We hypothesized that asprosin might led to vascular inflammation in hypertension via NLRP3 inflammasome formation. This study shows the importance of asprosin in the vascular inflammation of hypertension. Methods: Primary vascular smooth muscle cells (VSMCs) were obtained from the aorta of animals, including spontaneously hypertensive rats (SHR), Wistar-Kyoto rats (WKY), NLRP3(-/-) and wild-type mice. Studies were performed in VSMCs in vitro, as well as WKY and SHR in vivo. Results: Asprosin expressions were up-regulated in VSMCs and media of arteries in SHR. Asprosin overexpression promoted NLRP3 inflammasome activation via Toll-like receptor 4 (TLR4), accompanied with activation of NF kappa B signaling pathway in VSMCs. Exogenous asprosin protein showed similar roles in promoting NLRP3 inflammasome activation. Knockdown of asprosin restrained NLRP3 inflammasome and p65-NF kappa B activation in VSMCs of SHR. NLRP3 inhibitor MCC950 or NF kappa B inhibitor BAY11-7082 attenuated asprosin-caused VSMC proliferation and migration. Asprosin-induced interleukin-1 beta production, proliferation and migration were attenuated in NLRP3(-/-) VSMCs. Local asprosin knockdown in common carotid artery of SHR attenuated inflammation and vascular remodeling. Conclusions: Asprosin promoted NLRP3 inflammasome activation in VSMCs by TLR4-NF kappa B pathway, and thereby stimulates VSMCs proliferation, migration, and vascular remodeling of SHR.
Açıklama
Anahtar Kelimeler
Asprosin, Beh & Ccedil;Et'S Disease, Disease Activity, Uveitis, Vascular Inflammation
Kaynak
Journal of Clinical Laboratory Analysis
WoS Q Değeri
Q2
Scopus Q Değeri
Q1
