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While much research focuses on endogenous signaling pathways, extrinsic mechanismsparticularly the modulation of IBD through the gut microbiota-induced ferroptosis remain underexplored

1 Introduction Stroke remains the second-leading cause of death and disability worldwide, with ischemic stroke accounting for approximately 80% of cases ( First described in 2012, ferroptosis is characterized by mitochondrial cristae shrinkage, glutathione peroxidase 4 (GPX4) inactivation, and lethal lipid peroxide accumulation through iron-dependent Fenton reactions ( Emerging evidence identifies ferroptosis as a maladaptive response in stroke, with its unchecked activation exacerbating infarct volume expansion and worsening functional outcomes ( 2 Mechanisms of ferroptosis Ferroptosis is a distinct form of regulated cell death characterized by the accumulation of lipid peroxides to lethal levels ( The hallmark of ferroptosis lies in the peroxidation of polyunsaturated fatty acids within cellular membranes, driven by an imbalance between ROS and the cells antioxidant defense systems (Figure 1)

This exchange is crucial for the formation and maintenance of autophagosomes, which are responsible for sequestering and degrading selective cargo during autophagy [134, 135]

or an N-oxide, crystalline form, hydrate, or pharmaceutically acceptable salt thereof, with the proviso that: when R 3 is ethyl, R 1 and R 2 cannot be both H, O, or when R 3 is ethyl and at least one of R 1 or R 2 is H, R 1 or R 2 cannot be In one aspect of this embodiment, the compound has the structure of formula (II): R 3 is independently selected from the group consisting of H, C 1-12 aliphatic, C 1-6 -alkyl-aryl and C 1-6 -alkyl-heteroaryl

Dies betrifft nicht Arzneimittel mit den Wirkstoffen Cefi xim und Loracarbef