Results 71 to 80 of about 21,313 (286)
Intranasally administered hUMSC‐derived exosomes modulate the CRYAB–ARRDC3–Drp1 axis, alleviating mitochondrial dysfunction and ferroptosis, enhancing neuronal survival, reducing oxidative stress, and promoting functional recovery in ischemia‐reperfusion injury, offering a promising therapeutic strategy for ischemic stroke.
Rong ji +7 more
wiley +1 more source
Iron, Oxidative Damage and Ferroptosis in Rhabdomyosarcoma. [PDF]
Recent data have indicated a fundamental role of iron in mediating a non-apoptotic and non-necrotic oxidative form of programmed cell death termed ferroptosis that requires abundant cytosolic free labile iron to promote membrane lipid peroxidation ...
Fanzani, Alessandro, Poli, Maura
core +1 more source
We developed a novel copper‐doped aluminum nano‐adjuvant (CuNA) to overcome cytarabine resistance in acute myeloid leukemia (AML). CuNA effectively sensitizes drug‐resistant AML cells to cytarabine by inducing mitochondrial dysfunction and inhibiting HMGCR/GPX4 to amplify ferroptosis.
Chao He +10 more
wiley +1 more source
Molecular biology of glutathione peroxidase 4: from genomic structure to developmental expression and neural function [PDF]
Selenoproteins have been recognized as modulators of brain function and signaling. Phospholipid hydroperoxide glutathione peroxidase (GPx4/PHGPx) is a unique member of the selenium-dependent glutathione peroxidases in mammals with a pivotal role in brain
Borchert, Astrid +3 more
core
CypD Dependent mPTP Opening Is Crucial for Oxidized Mitochondrial DNA Release in Ferroptosis
Ferroptosis is driven by mitochondrial permeability transition pore (mPTP) opening, which induces mitochondrial swelling and releases oxidized mitochondrial DNA. The released mtDNA activates cGAS–STING signaling, promotes ferritinophagy, and amplifies ferroptotic cell death. Disruption of mtDNA repair sensitizes tumors to ferroptosis in vivo, revealing
Hong Zhou +5 more
wiley +1 more source
Ferroptosis has been observed during retinal photoreceptor cell death, suggesting that it plays a role in retinitis pigmentosa (RP) pathogenesis.
Meng Xiong +8 more
doaj +1 more source
A possible role for selenoprotein glutathione peroxidase (GPx1) and thioredoxin reductases (TrxR1) in thyroid cancer. Our experience in thyroid surgery [PDF]
Background: Oxidative stress is responsible for some alterations in the chemical structure and, consequently, in the function of proteins, lipids, and DNA.
DE LUCA, Alessandro +6 more
core +2 more sources
Aldosterone‐producing adenomas (APAs) develop via two distinct paths: directly from adrenal zona glomerulosa (zG) cells, or stepwise from zG cells through aldosterone‐producing micronodules (APMs) before progressing to APAs. Advanced single‐cell and spatial analyses identified distinct cell states linked to oxidative stress and cell–cell interactions ...
Zhuolun Sun +7 more
wiley +1 more source
CoQ deficiency causes disruption of mitochondrial sulfide oxidation, a new pathomechanism associated with this syndrome [PDF]
Coenzyme Q (CoQ) is a key component of the mitochondrial respiratory chain, but it also has several other functions in the cellular metabolism. One of them is to function as an electron carrier in the reaction catalyzed by sulfide:quinone oxidoreductase (
Barriocanal-Casado, Eliana +5 more
core +4 more sources
The ultra‐short‐acting sedative remimazolam has a sustained therapeutic effect on the core symptoms of VPA‐exposed mice. Remimazolam, a GABA agonist, exerts its therapeutic effects by protecting dopamine neurons in the VTA of VPA‐exposed mice. Meanwhile, ferroptosis is the critical mechanism by which remimazolam protects VTA dopaminergic neurons and ...
Yuxin Zhang +7 more
wiley +1 more source

