Targeting epigenetic and posttranslational modifications regulating ferroptosis for the treatment of diseases

Signal Transduction and Targeted Therapy, Journal Year: 2023, Volume and Issue: 8(1)

Published: Dec. 10, 2023

Abstract Ferroptosis, a unique modality of cell death with mechanistic and morphological differences from other modes, plays pivotal role in regulating tumorigenesis offers new opportunity for modulating anticancer drug resistance. Aberrant epigenetic modifications posttranslational (PTMs) promote resistance, cancer progression, metastasis. Accumulating studies indicate that can transcriptionally translationally determine vulnerability to ferroptosis functions as driver nervous system diseases (NSDs), cardiovascular (CVDs), liver diseases, lung kidney diseases. In this review, we first summarize the core molecular mechanisms ferroptosis. Then, roles processes, including histone PTMs, DNA methylation, noncoding RNA regulation such phosphorylation, ubiquitination, SUMOylation, acetylation, ADP-ribosylation, are concisely discussed. The PTMs genesis cancers, NSD, CVDs, well application PTM modulators therapy these then discussed detail. Elucidating mediated by will facilitate development promising combination therapeutic regimens containing or PTM-targeting agents inducers be used overcome chemotherapeutic resistance could prevent addition, highlight potential approaches chemoresistance halt

Language: Английский

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Fine particulate matter (PM2.5) induces testosterone disruption by triggering ferroptosis through SIRT1/HIF-1α signaling pathway in male mice

Free Radical Biology and Medicine, Journal Year: 2024, Volume and Issue: 221, P. 40 - 51

Published: May 15, 2024

Language: Английский

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Ferroptosis induced by environmental pollutants and its health implications

Cell Death Discovery, Journal Year: 2025, Volume and Issue: 11(1)

Published: Jan. 24, 2025

Abstract Environmental pollution represents a significant public health concern, with the potential risks associated environmental pollutants receiving considerable attention over an extended period. In recent years, substantial body of research has been dedicated to this topic. Since discovery ferroptosis, iron-dependent programmed cell death typically characterized by lipid peroxidation, in 2012, there have advances study its role and mechanism various diseases. A growing number studies also demonstrated involvement ferroptosis damage caused organism pollutants, molecular mechanisms involved partially elucidated. The targeting be effective means ameliorating PM2.5, organic inorganic ionizing radiation. This review begins providing summary most important ferroptosis. It then proceeds offer critical analysis effects induced pollutants. Furthermore, as is case all rapidly evolving areas, are numerous unanswered questions challenges pertaining pollutant-induced which we discuss attempt provide some directions clues for future field.

Language: Английский

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Melatonin ameliorates PM2.5-induced airway inflammation and apoptosis by PERK/eIF2α/ATF4/CHOP in chronic obstructive pulmonary disease mice

Toxicology and Applied Pharmacology, Journal Year: 2025, Volume and Issue: unknown, P. 117314 - 117314

Published: March 1, 2025

Language: Английский

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Melatonin and ferroptosis: Mechanisms and therapeutic implications

Biochemical Pharmacology, Journal Year: 2023, Volume and Issue: 218, P. 115909 - 115909

Published: Nov. 4, 2023

Language: Английский

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Cellular Senescence: A Troy Horse in Pulmonary Fibrosis

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(22), P. 16410 - 16410

Published: Nov. 16, 2023

Pulmonary fibrosis (PF) is a chronic interstitial lung disease characterized by myofibroblast abnormal activation and extracellular matrix deposition. However, the pathogenesis of PF remains unclear, treatment options are limited. Epidemiological studies have shown that average age patients estimated to be over 65 years, incidence increases with age. Therefore, considered an age-related disease. A preliminary study on demonstrated combination therapy anti-senescence drugs dasatinib quercetin improved physical functional indicators. Given global aging population role cellular senescence in tissue organ aging, understanding impact growing interest. This article systematically summarizes causes signaling pathways PF. It also objectively analyzes AECs fibroblasts development. Furthermore, potential intervention methods targeting discussed. review not only provides strong theoretical foundation for manipulating senescence, developing new therapies improve diseases, extending healthy lifespan but offers hope reversing toxicity caused massive accumulation cells humans.

Language: Английский

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Mangiferin alleviates diabetic pulmonary fibrosis in mice via inhibiting endothelial-mesenchymal transition through AMPK/FoxO3/SIRT3 axis

Acta Pharmacologica Sinica, Journal Year: 2024, Volume and Issue: 45(5), P. 1002 - 1018

Published: Jan. 15, 2024

Language: Английский

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Ferroptosis in organ fibrosis: From mechanisms to therapeutic medicines

Journal of Translational Internal Medicine, Journal Year: 2024, Volume and Issue: 12(1), P. 22 - 34

Published: Feb. 1, 2024

Abstract Fibrosis occurs in many organs, and its sustained progress can lead to organ destruction malfunction. Although numerous studies on fibrosis have been carried out, underlying mechanism is largely unknown, no ideal treatment currently available. Ferroptosis an iron-dependent process of programmed cell death that characterized by lipid peroxidation. In the past decade, a growing body evidence demonstrated association between ferroptosis fibrotic diseases, while targeting may serve as potential therapeutic strategy. This review highlights recent advances crosstalk fibrosis, discusses ferroptosis-targeted approaches against are being explored.

Language: Английский

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Melatonin: a ferroptosis inhibitor with potential therapeutic efficacy for the post-COVID-19 trajectory of accelerated brain aging and neurodegeneration

Molecular Neurodegeneration, Journal Year: 2024, Volume and Issue: 19(1)

Published: April 19, 2024

Abstract The unprecedented pandemic of COVID-19 swept millions lives in a short period, yet its menace continues among survivors the form post-COVID syndrome. An exponentially growing number suffer from cognitive impairment, with compelling evidence trajectory accelerated aging and neurodegeneration. novel enigmatic nature this yet-to-unfold pathology demands extensive research seeking answers for both molecular underpinnings potential therapeutic targets. Ferroptosis, an iron-dependent cell death, is strongly proposed underlying mechanism post-COVID-19 neurodegeneration discourse. incites neuroinflammation, iron dysregulation, reactive oxygen species (ROS) accumulation, antioxidant system repression, renin-angiotensin (RAS) disruption, clock gene alteration. These events pave way ferroptosis, which shows signature COVID-19, premature aging, neurodegenerative disorders. In search treatment, melatonin shines as promising ferroptosis inhibitor repeatedly reported safety tolerability. According to various studies, has proven efficacy attenuating severity certain manifestations, validating reputation anti-viral compound. Melatonin well-documented anti-aging properties combating neurodegenerative-related pathologies. can block leading since it efficient anti-inflammatory, chelator, antioxidant, angiotensin II antagonist, regulator. Therefore, we propose culprit behind melatonin, well-fitting inhibitor, treatment.

Language: Английский

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FGF10 protects against particulate matter-induced lung injury by inhibiting ferroptosis via Nrf2-dependent signaling

International Immunopharmacology, Journal Year: 2024, Volume and Issue: 134, P. 112165 - 112165

Published: May 1, 2024

Language: Английский

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