Lipoxin A₄ suppresses angiotensin II type 1 receptor autoantibody in preeclampsia via modulating caspase-1.

ABSTRACT: Preeclampsia (PE) remains a leading cause of maternal and neonatal morbidity and mortality. Numerous studies have shown that women with PE develop autoantibody, termed angiotensin II type 1 receptor autoantibody (AT1-AA), and key features of the disease result from it. Emerging evidence has indicated that inflammatory cell necrosis, such as pyroptosis, could lead to autoantigen exposure and stimulate autoantibody production. Caspase-1, the central enzyme of inflammasome and key target of pyroptosis, may play roles in AT1R exposure and AT1-AA production. Exploring endogenous regulator that could inhibit AT1-AA production by targeting pyroptosis will be essential for treating PE. Lipoxin A₄ (LXA₄), endogenous dual anti-inflammatory and proresolving lipid mediator, may i

SUBMITTER: Liu H 

PROVIDER: S-EPMC6992755 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature