GPX4, GSH and Stroke Reduced GSH is an important co-factor in the scavenging of membrane lipid peroxides by glutathione peroxidase 4 (GPX4), thereby reducing oxidative stress ( in vivo and in vitro, overexpression of GPX4 significantly reduced lipid peroxidation in neurons, improved brain edema and neurological impairment after SAH, and showed critical protection of the brain ( As one of the key regulators of ferroptosis, GSH not only functions in an auxiliary capacity in the activity of GPX4 but is also the only remaining ligand of Fe 2+ in cells that can block the Fenton reaction and reduce the production of highly toxic hydroxyl radicals so as to inhibit ferroptosis ( Lipid Peroxidation in Stroke LOX and Stroke LOX is a key enzyme that catalyzes lipid peroxidation and ferroptosis caused by polyunsaturated fatty acids (PUFAs) in phospholipid membranes ( ACSL4 and Stroke ACSL4 shapes the lipid composition of cells, affects the synthesis of lipid peroxides, and determines the sensitivity of cells to ferroptosis ( Crosstalk Between Ferroptosis and Other Pathologic Processes in Stroke Brain injury caused by stroke manifests multiple factors, mechanisms, and linkages in the malignant cascade process
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The core components of the mammalian Hippo pathway include the upstream large tumor suppressor (LATS) kinases (LATS1 and LATS2), mammalian Ste20-like kinases 1/2 (MST1/2), the scaffolding protein Salvador (SAV/WW45) corresponding to LATS and MST, scaffolding protein MOB domain kinase activator 1A/B (MOB1A/B), and two downstream transcriptional coactivators Yes-associated protein (YAP) and transcriptional coactivator of PDZ-binding motif (TAZ)
Allicin has the property to enhance cognitive function through restoring neurotransmitter levels, regulating microglial activity and decreasing neuroinflammation (83)
Amyotrophic lateral sclerosis and metabolomics: Clinical implication and therapeutic approach
