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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Emerging roles of ferroptosis in pulmonary fibrosis: current perspectives, opportunities and challenges

Cell Death Discovery, Journal Year: 2024, Volume and Issue: 10(1)

Published: June 24, 2024

Abstract Pulmonary fibrosis (PF) is a chronic interstitial lung disorder characterized by abnormal myofibroblast activation, accumulation of extracellular matrix (ECM), and thickening fibrotic alveolar walls, resulting in deteriorated function. PF initiated dysregulated wound healing processes triggered factors such as excessive inflammation, oxidative stress, coronavirus disease (COVID-19). Despite advancements understanding the disease’s pathogenesis, effective preventive therapeutic interventions are currently lacking. Ferroptosis, an iron-dependent regulated cell death (RCD) mechanism involving lipid peroxidation glutathione (GSH) depletion, exhibits unique features distinct from other RCD forms (e.g., apoptosis, necrosis, pyroptosis). Imbalance between reactive oxygen species (ROS) production detoxification leads to ferroptosis, causing cellular dysfunction through peroxidation, protein modifications, DNA damage. Emerging evidence points crucial role ferroptosis progression, driving macrophage polarization, fibroblast proliferation, ECM deposition, ultimately contributing tissue scarring. This review provides comprehensive overview latest findings on involvement signaling mechanisms emphasizing potential novel anti-fibrotic approaches targeting for management.

Language: Английский

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The potential roles of HIF-1α in epithelial-mesenchymal transition and ferroptosis in tumor cells

Cellular Signalling, Journal Year: 2024, Volume and Issue: 122, P. 111345 - 111345

Published: Aug. 10, 2024

In tumors, the rapid proliferation of cells and imperfect blood supply system lead to hypoxia, which can regulate adaptation tumor hypoxic environment through hypoxia-inducible factor-1α (HIF-1α) promote development in multiple ways. Recent studies have found that epithelial-mesenchymal transition (EMT) ferroptosis play important roles progression cells. The activation HIF-1α is considered a key factor inducing EMT When activated, it EMT-related genes, causing gradually lose their epithelial characteristics acquire more invasive mesenchymal traits. occurrence allows better adapt changes surrounding tissue, enhancing migratory capabilities, thus promoting progression. At same time, also plays crucial regulatory role environment, may affect processes such as iron metabolism oxidative stress responses, This article briefly reviews dual cells, helping gain deeper understanding pathways providing new perspective for pathogenesis tumors. regulation become an strategy future therapy.

Language: Английский

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Metal ions overloading and cell death

Cell Biology and Toxicology, Journal Year: 2024, Volume and Issue: 40(1)

Published: Aug. 20, 2024

Cell death maintains cell morphology and homeostasis during development by removing damaged or obsolete cells. The concentration of metal ions whithin cells is regulated various intracellular transporters repositories to maintain dynamic balance. External internal stimuli might increase the ions, which results in overloading. Abnormal accumulation large amounts can lead disruption signaling cell, turn produce toxic effects occurrence different types deaths. In order further study overloading induced death, this paper reviewed regulation Ca2+, Fe3+, Cu2+ Zn2+ mechanism Furthermore, we found that possess a synergistic competitive relationship death. And enhanced level oxidative stress was present all processes due overloading, possibly combination factors. Therefore, review offers theoretical foundation for investigation presents innovative insights targeted therapeutic intervention. • Metal disrupts homeostasis, affects cause via reactive oxygen species (ROS). Different have relationships regulating

Language: Английский

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Targeting iron-metabolism:a potential therapeutic strategy for pulmonary fibrosis

Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 172, P. 116270 - 116270

Published: Feb. 15, 2024

Iron homeostasisis is integral to normal physiological and biochemical processes of lungs. The maintenance iron homeostasis involves the process intake, storage output, dependening on iron-regulated protein/iron response element system operate tightly metabolism-related genes, including TFR1, DMT1, Fth, FPN. Dysregulation can lead overload, which increases virulence microbial colonisers occurrence oxidative stress, causing alveolar epithelial cells undergo necrosis apoptosis, form extracellular matrix. Accumulated drive iron-dependent ferroptosis exacerbated pulmonary fibrosis. Notably, chelator deferoxamine lipophilic antioxidant ferritin-1 have been shown attenuate inhibit lipid peroxidation in paper summarises regulatory mechanisms dysregulated metabolism development Targeting may be a potential therapeutic strategy for prevention treatment

Language: Английский

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