NHE1 in macrophages promotes octanal/Olfr2-induced atherosclerosis via calcium-dependent ROS and NLRP3 inflammasome activation.

ABSTRACT: Atherosclerosis (AS) is the leading cause of global mortality and morbidity. Despite the elevated expression of sodium-hydrogen exchanger 1 (NHE1) and olfactory receptor 2 (Olfr2) in plaque macrophages, their interactions within the AS context remain poorly understood. In this study, ApoE^-/- mice and RAW264.7 macrophages were employed to examine the impact of intraperitoneal octanal injection on atherosclerosis and NHE1 expression in vivo. In vitro analyses were conducted to assess NHE1 expression, activity, and inflammatory responses subsequent to treatment with octanal and an NHE1 inhibitor. Furthermore, the underlying mechanisms were investigated through RNA interference and calcium ion (Ca2+) chelation. In vivo, octanal aggravated AS by upregulating NHE1 within plaques, whil

SUBMITTER: Wang T 

PROVIDER: S-EPMC12749899 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature