CircMAPK1 induces cell pyroptosis in sepsis-induced lung injury by mediating KDM2B mRNA decay to epigenetically regulate WNK1.

Background: Macrophage pyroptosis is a pivotal inflammatory mechanism in sepsis-induced lung injury, however, the underlying mechanisms remain inadequately elucidated.

Methods: Lipopolysaccharides (LPS)/adenosine triphosphate (ATP)-stimulated macrophages and cecal ligation and puncture (CLP)-induced mouse model for sepsis were established. The levels of key molecules were examined by qRT-PCR, Western blotting, immunohistochemistry (IHC) and ELISA assay.

miR-122-3p Alleviates LPS-Induced Pyroptosis of Macrophages via Targeting NLRP1.

Objective: Sepsis, a life-threatening organ dysfunction, is among the leading causes of mortality in intensive care units. Sepsis occurrence is associated with macrophage pyroptosis, and microRNAs (miRNAs) have emerged as key factors in this process. However, the specific role of miR-122-3p in pyroptosis during sepsis progression and its underlying mechanisms remain to be fully elucidated.

Formation of perfluorocarboxylic acids (PFCAs) during the exposure of earthworms to 6:2 fluorotelomer sulfonic acid (6:2 FTSA).

6:2 fluorotelomer sulfonic acid (6:2 FTSA) is a novel perfluorooctane sulfonate (PFOS) alternative used globally in aqueous film forming foams (AFFFs). Although 6:2 FTSA has been recently detected in the environment, its fate in terrestrial invertebrates remains unclear. The uptake, elimination and biotransformation of 6:2 FTSA in earthworms (Eisenia fetida) were investigated after in vivo and in vitro exposure.