Fig. 1: Ferroptosis, lipid peroxidation, and acute pancreatitis. | Cell Death Discovery

Fig. 1: Ferroptosis, lipid peroxidation, and acute pancreatitis.

From: Ferroptosis exacerbates hyperlipidemic acute pancreatitis by enhancing lipid peroxidation and modulating the immune microenvironment

Fig. 1

During enzymatic lipid peroxidation, free unsaturated fatty acids are anchored and lengthened at the cell membrane by ACSL4 and LPCAT3, and newly produced long-chain unsaturated fatty acids enter the cytosol to cause calcium overload, which exacerbates pancreatic injury by decreasing ATP production, inducing inflammatory responses, and activating pancreatic enzyme pathways at inappropriate times. In addition, ALOX5 catalyzes the binding of free iron ions to unsaturated fatty acids and the gradual production of inflammatory mediators such as LTs to exacerbate the severity of AP. During nonenzymatic lipid peroxidation, the catabolic products of unsaturated phospholipids use the Fenton reaction to increase cell membrane damage and inappropriately activate pancreatic enzymes to cause SAP (PUFA, polyunsaturated fatty acid; ACSL4, acyl-CoA synthetase long-chain family member 4; LPCAT3, lysophosphatidylcholine acyltransferase 3; AA, arachidonic acid; ALOX5, arachidonate-5-lipoxygenase; 5-HPETE, 5-hydroperoxyeicosatetraenoic acid; LT, leukotriene; PLOO-, phospholipid peroxyl radical; PLOOH, phospholipid hydroperoxide).

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