Ferroptosis Signaling Pathways: Alzheimer's Disease

Horm Metab Res DOI: 10.1055/a-2084-3561The involvements of iron metabolism, lipid peroxidation, and oxidative stress in
Alzheimer's disease (AD) development have recently received a lot of
attention. We also observe that these pathogenic occurrences play a key role in
regulating ferroptosis, a unique regulatory cell death that is iron-dependent,
oxidative, and non-apoptotic. Iron is a crucial component that makes up a
subunit of the oxidase responsible for lipid peroxidation. A family of non-heme
iron enzymes known as lipoxygenases (LOXs) can cause ferroptosis by oxidising
polyunsaturated fatty acids in cellular membranes (PUFAs). Toxic lipid
hydroperoxides are produced in large part by the iron in LOX active sites.
Deferoxamine and deferiprone, two iron chelators, could also treat ferroptosis
by eliminating the crucial catalytic iron from LOXs. Phospholipids containing
polyunsaturated fatty acids are the main substrates of lipid peroxidation in
ferroptosis, which is favourably controlled by enzymes like ACSL4, LPCAT3,
ALOXs, or POR. Selective stimulation of autophagic degradation pathways leads to
an increase in iron accumulation and lipid peroxidation, which promotes
ferroptosis. We highlighted recent advancements in our understanding of
ferroptosis signaling routes in this study. One form of regulated necrotic cell
...

Source: Hormone and Metabolic Research - May 31, 2023 Category: Endocrinology Authors: Maheshwari, Shubhrat Tags: Review Source Type: research