Ferroptosis: iron release mechanisms in the bioenergetic process

Cancer and Metastasis Reviews, Год журнала: 2025, Номер 44(1)

Опубликована: Фев. 25, 2025

Язык: Английский

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Xenotopic synthetic biology: Prospective tools for delaying aging and age-related diseases

Science Advances, Год журнала: 2025, Номер 11(13)

Опубликована: Март 28, 2025

Metabolic dysregulation represents one of the major driving forces in aging. Although multiple genetic and pharmacological manipulations are known to extend longevity model organisms, aging is a complex trait, targeting one’s own genes may be insufficient prevent age-dependent deterioration. An alternative strategy could use enzymes from other species reverse age-associated metabolic changes. In this review, we discuss set lower organisms that have been shown affect various parameters linked age-related processes. These include modulators steady-state levels amino acids (METase, ASNase, ADI), NADPH/NADP + and/or reduced form coenzyme Q (CoQH 2 )/CoQ redox potentials (NDI1, AOX, Lb NOX, TPNOX, Ec STH, RquA, LOXCAT, Grubraw, ScURA), GSH (StGshF), mitochondrial membrane potential (mtON mito-dR), or reactive oxygen (DAAO KillerRed-SOD1). We propose leveraging non-mammalian an untapped resource can used delay diseases.

Язык: Английский

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The perspective of targeting cancer cell metabolism: combination therapy approaches

Molecular Biology Reports, Год журнала: 2025, Номер 52(1)

Опубликована: Апрель 9, 2025

Язык: Английский

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Circular RNA-encoded oncogenic PIAS1 variant blocks immunogenic ferroptosis by modulating the balance between SUMOylation and phosphorylation of STAT1

Molecular Cancer, Год журнала: 2024, Номер 23(1)

Опубликована: Сен. 28, 2024

Язык: Английский

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Inhibition of mitochondrial complex I induces mitochondrial ferroptosis by regulating CoQH2 levels in cancer

Cell Death and Disease, Год журнала: 2025, Номер 16(1)

Опубликована: Апрель 5, 2025

Abstract Ferroptosis, a novel form of regulated cell death induced by the excessive accumulation lipid peroxidation products, plays pivotal role in suppression tumorigenesis. Two prominent mitochondrial ferroptosis defense systems are glutathione peroxidase 4 (GPX4) and dihydroorotate dehydrogenase (DHODH), both which localized within mitochondria. However, existence supplementary cellular mechanisms against remains unclear. Our findings unequivocally demonstrate that inactivation respiratory chain complex I (MCI) induces consequently invokes across GPX4 low-expression cancer cells. high expression cells, MCI inhibitor did not induce ferroptosis, but increased sensitivity to inhibitor. Overexpression alternative protein yeast NADH-ubiquinone reductase (NDI1) only quells inhibitors also confers protection inducers. Mechanically, actuate an elevation NADH level while concomitantly diminishing CoQH2 level. The manifestation inhibitor-induced can be reversed supplementation with mitochondrial-specific analogues CoQH2. Notably, operates parallel mitochondrial-localized DHODH inhibit independently cytosolically or suppressor 1(FSP1). IACS-010759, is endowed ability concurrently impeding tumor proliferation vivo. results identified mechanism mediated mitochondria suggested therapeutic strategy for targeting treatment.

Язык: Английский

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Summary of the mechanism of ferroptosis regulated by m6A modification in cancer progression

Frontiers in Cell and Developmental Biology, Год журнала: 2025, Номер 13

Опубликована: Апрель 9, 2025

The most common form of internal RNA modification in eukaryotes is called n6-methyladenosine (m6A) methylation. It has become more and well-known as a research issue recent years since it alters metabolism involved numerous biological processes. Currently, m6A alteration offers new opportunities clinical applications intimately linked to carcinogenesis. Ferroptosis-a iron-dependent, lipid peroxidation-induced regulated cell death-was discovered. In the development cancer, an important factor. According newly available data, ferroptosis regulates tumor growth, cancer exhibits aberrant levels crucial regulatory components. On other hand, multiple roles tumors, relationship between m6A-modified malignancies quite intricate. this review, we first give thorough review functional methylation, focusing on molecular processes through regulation human progression metastasis, which are strongly associated initiation, progression, drug resistance. Therefore, clarify m6A-mediated providing strategy for treatment with substantial implications.

Язык: Английский

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Ferroptosis: a novel mechanism of cell death in ophthalmic conditions

Frontiers in Immunology, Год журнала: 2024, Номер 15

Опубликована: Июнь 27, 2024

Ferroptosis, a new type of programmed cell death proposed in recent years, is characterized mainly by reactive oxygen species and iron-mediated lipid peroxidation differs from death, such as apoptosis, necrosis, autophagy. Ferroptosis associated with variety physiological pathophysiological processes. Recent studies have shown that ferroptosis can aggravate or reduce the occurrence development diseases targeting metabolic pathways signaling tumors, ischemic organ damage, other degenerative related to peroxidation. Increasing evidence suggests closely linked onset progression various ophthalmic conditions, including corneal injury, glaucoma, age-related macular degeneration, diabetic retinopathy, retinal detachment, retinoblastoma. Our review current research on reveals significant advancements our understanding pathogenesis, aetiology, treatment these conditions.

Язык: Английский

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NDUFS3 alleviates oxidative stress and ferroptosis in sepsis induced acute kidney injury through AMPK pathway

International Immunopharmacology, Год журнала: 2024, Номер 143, С. 113393 - 113393

Опубликована: Окт. 18, 2024

Язык: Английский

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Gingerenone A induces ferroptosis in colorectal cancer via targeting suppression of SLC7A11 signaling pathway

Biomedicine & Pharmacotherapy, Год журнала: 2024, Номер 180, С. 117529 - 117529

Опубликована: Окт. 10, 2024

Язык: Английский

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WBP1 regulates mitochondrial function and ferroptosis to modulate chemoresistance in colorectal cancer

Molecular Medicine, Год журнала: 2025, Номер 31(1)

Опубликована: Март 12, 2025

Abstract Chemoresistance continues to pose a significant challenge in managing colorectal cancer (CRC), resulting unfavorable outcomes for patients. Recent findings indicate that ferroptosis, an innovative type of regulated cell death, might influence chemoresistance. In this research, we explored how WW domain-binding protein 1 (WBP1) affects mitochondrial function, growth, and chemoresistance CRC cells. By employing both genetic pharmacological methods, found WBP1 is essential maintaining respiration depletion impaired leading reduced proliferation increased ferroptosis. Exogenous mitochondria from wild-type cells restored proliferation, suppressed ferroptosis WBP1-deficient cells, indicating function acts downstream WBP1. Importantly, demonstrated targeting or its mediated sensitized chemoresistant 5-fluorouracil oxaliplatin by inducing Furthermore, analyzed transcriptome data patients, which indicated expression correlated with poor patients receiving chemotherapy, thus highlighting the clinical significance our observations. Collectively, results pinpoint as modulator imply may represent viable approach tackling These insights offer deeper understanding molecular pathways underlying guide development new treatment options.

Язык: Английский

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