The accumulation of lipid droplets, rich in polyunsaturated fatty acids (PUFAs), also creates vulnerability to ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation [18, 19]
1 Introduction Ferroptosis is an iron-dependent regulated cell death driven by the peroxidation damage of phospholipid-containing polyunsaturated fatty acyl tails (PUFA-PLs) on the cell membrane or organelle membrane and subsequent membrane rupture ( Herein, we summarize the processes of ferroptosis in glioma, the current findings on ferroptosis in glioma, which include some of the pivotal regulators and pathways relevant to ferroptosis and the crosstalk between ferroptosis and other programmed cell death including apoptosis, autophagic cell death, necroptosis and pyroptosis
Inflammation is a defensive reaction of the body that arises after microbial invasion, exposure to antigens, or cellular and tissue injury
Prostaglandin E2 (PGE2), the most important bioactive mediator secreted by neutrophils, accelerates blood flow and produces oedema and pain, and its synthesis is primarily related to AA, which is related to LDs (Kawahara et al., 2015)
