Ferritinophagy mediated by the AMPK/ULK1 pathway is involved in ferroptosis subsequent to ventilator-induced lung injury.

Mechanical ventilation (MV) remains a cornerstone of critical care; however, its prolonged application can exacerbate lung injury, leading to ventilator-induced lung injury (VILI). Although previous studies have implicated ferroptosis in the pathogenesis of VILI, the underlying mechanisms remain unclear. This study investigated the roles of ferritinophagy in ferroptosis subsequent to VILI.

Ferrostatin-1 alleviates ventilator-induced lung injury by inhibiting ferroptosis.

Ventilator-induced lung injury (VILI) has become an increasingly common complication in the clinic concerning mechanical ventilation. Previous research showed that VILI is the result of a response to cascade inflammation; however, the inflammatory mechanism involved remains unclear. As a newly recognized form of cell death, ferroptosis can release damage-related molecules (DAMPs) to trigger and amplify the inflammatory response and is involved in several inflammatory diseases.

Identification of hub genes associated with acute kidney injury induced by renal ischemia-reperfusion injury in mice.

Acute kidney injury (AKI) is a severe clinical syndrome, and ischemia-reperfusion injury is an important cause of acute kidney injury. The aim of the present study was to investigate the related genes and pathways in the mouse model of acute kidney injury induced by ischemia-reperfusion injury (IRI-AKI). Two public datasets (GSE39548 and GSE131288) originating from the NCBI Gene Expression Omnibus (GEO) database were analyzed using the R software limma package, and differentially expressed genes (DEGs) were identified.

Inhibition of IP3R/Ca2+ Dysregulation Protects Mice From Ventilator-Induced Lung Injury Endoplasmic Reticulum and Mitochondrial Pathways.

Rationale: Disruption of intracellular calcium (Ca2+) homeostasis is implicated in inflammatory responses. Here we investigated endoplasmic reticulum (ER) Ca2+ efflux through the Inositol 1,4,5-trisphosphate receptor (IP3R) as a potential mechanism of inflammatory pathophysiology in a ventilator-induced lung injury (VILI) mouse model.

Methods: C57BL/6 mice were exposed to mechanical ventilation using high tidal volume (HTV).

TLR4/TRAF6/NOX2 signaling pathway is involved in ventilation-induced lung injury via endoplasmic reticulum stress in murine model.

In ventilation-induced lung injury (VILI), prolonged nonpathogen-mediated inflammation is triggered as a result of alveolar hyperinflation. In our previous study, we suggested that endoplasmic reticulum (ER) stress-mediated inflammation was involved in VILI, but how ER stress is triggered remains unknown. Toll-like receptor 4 (TLR4) activation plays an important role in mechanical ventilation (MV)-induced lung inflammation, however, it is unknown whether ER stress is activated by TLR4 to participate in VILI.