Ferroptosis in pulmonary fibrosis: an emerging therapeutic target DOI Creative Commons
Chunyan Wang, Shucheng Hua, Lei Song

et al.

Frontiers in Physiology, Journal Year: 2023, Volume and Issue: 14

Published: Aug. 17, 2023

In recent years, the role of ferroptosis in pulmonary fibrosis has garnered increasing interest as a potential therapeutic target. Pulmonary is pathological process characterized by accumulation extracellular matrix affected lung tissues, and currently, there are no effective therapies for preventing or reversing fibrotic lesions. Ferroptosis form programmed cell death that regulated network enzymes signaling pathways. Dysregulation been implicated several diseases, including fibrosis. The lipid peroxides course causes damage to membranes other cellular components, leading ultimately death. Relevant targets intervention include key enzymes, such glutathione peroxidase 4, transcription factors like nuclear factor erythroid 2-related 2, iron chelation. This review provides an overview emerging highlights this pathway. Further research needed develop safe approaches targeting treatment

Language: Английский

Ferroptosis induced by environmental pollutants and its health implications DOI Creative Commons
Fu‐Han Gong, Liyuan Liu,

Xuesheng Wang

et al.

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

Citations

1
Hesperetin alleviates PM2.5-induced lung injury by inhibiting ferroptosis in an Nrf2-dependent manner DOI
Lu Wang, Ying Tang,

Tianhua Hou

et al.

International Immunopharmacology, Journal Year: 2025, Volume and Issue: 148, P. 114123 - 114123

Published: Jan. 29, 2025

Language: Английский

Citations

1
Ferroptosis in Pulmonary Disease and Lung Cancer: Molecular Mechanisms, Crosstalk Regulation, and Therapeutic Strategies DOI Creative Commons
Dandan Guo, Songhua Cai,

Lvdan Deng

et al.

MedComm, Journal Year: 2025, Volume and Issue: 6(3)

Published: Feb. 23, 2025

Ferroptosis is a distinct form of iron-dependent programmed cell death characterized primarily by intracellular iron accumulation and lipid peroxidation. Multiple cellular processes, including amino acid metabolism, various signaling pathways, autophagy, have been demonstrated to influence the induction progression ferroptosis. Recent investigations elucidated that ferroptosis plays crucial role in pathogenesis pulmonary disorders, lung injury, chronic obstructive disease, fibrosis, asthma. increasingly recognized as promising novel strategy for cancer treatment. Various immune cells within tumor microenvironment, CD8+ T cells, macrophages, regulatory natural killer dendritic shown induce modulate process through regulation metabolism pathways. Conversely, can reciprocally alter metabolic environment, leading activation or inhibition functions, thereby modulating responses. This paper reviews molecular mechanism describes discusses connection between microenvironment diseases, development prospect their interaction treatment diseases.

Language: Английский

Citations

1
PM2.5 regulates TGF-β1/Smads-mediated pulmonary fibrosis via ROS/SnoN in vitro and in vivo DOI
Xiaohong Li, Xuan Ma, Limin Zhang

et al.

International Immunopharmacology, Journal Year: 2025, Volume and Issue: 153, P. 114477 - 114477

Published: March 29, 2025

Language: Английский

Citations

1
Ferroptosis in organ fibrosis: From mechanisms to therapeutic medicines DOI Creative Commons

Weijing Lai,

Bo Wang,

Rongshuang Huang

et al.

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

Citations

8
HOXD10 attenuates renal fibrosis by inhibiting NOX4-induced ferroptosis DOI Creative Commons
Xin Li,

Tian‐Kui Ma,

Pu Wang

et al.

Cell Death and Disease, Journal Year: 2024, Volume and Issue: 15(6)

Published: June 6, 2024

Abstract In chronic kidney disease (CKD), renal fibrosis is an unavoidable result of various manifestations. However, its pathogenesis not yet fully understood. Here, we revealed the novel role Homeobox D10 (HOXD10) in CKD-related fibrosis. HOXD10 expression was downregulated vitro and vivo models. UUO model mice were administered adeno-associated virus (AAV) containing HOXD10, overexpression plasmids introduced into human proximal tubular epithelial cells induced by TGF-β1. The levels iron, reactive oxygen species (ROS), lipid ROS, oxidized glutathione/total glutathione (GSSG/GSH) ratio, malonaldehyde (MDA), superoxide dismutase (SOD) determined using respective assay kits. Treatment with AAV–HOXD10 significantly attenuated dysfunction inhibiting NOX4 transcription, ferroptosis pathway activation, oxidative stress. High activation profibrotic gene TGF-β1/erastin (a agonist) abrogated HK-2 cells. Moreover, bisulfite sequencing PCR that showed a hypermethylated level TGF-β1-treated binding to promoter confirmed chromatin immunoprecipitation (ChIP) analysis dual-luciferase reporter assays. Targeting may represent innovative therapeutic strategy for treatment CKD.

Language: Английский

Citations

8
Emerging roles of ferroptosis in pulmonary fibrosis: current perspectives, opportunities and challenges DOI Creative Commons
Yixiang Hu,

Ying Huang,

Lijuan Zong

et al.

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

Citations

8
Targeting iron-metabolism:a potential therapeutic strategy for pulmonary fibrosis DOI Open Access
Yi Sun,

Yu Ren,

Liyun Song

et al.

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

Citations

7
PM2.5 Induces Cardiomyoblast Senescence via AhR-Mediated Oxidative Stress DOI Creative Commons
Tiantian Liu, Bin Jiang,

Baoqiang Fu

et al.

Antioxidants, Journal Year: 2024, Volume and Issue: 13(7), P. 786 - 786

Published: June 28, 2024

Previous research has established a correlation between PM2.5 exposure and aging-related cardiovascular diseases, primarily in blood vessels. However, the impact of on cardiomyocyte aging remains unclear. In this study, we observed that extractable organic matter (EOM) from led to cellular senescence H9c2 cardiomyoblast cells, as characterized by an increase percentage β-galactosidase-positive elevated expression levels p16 p21, enhanced H3K9me3 foci. EOM also induced cell cycle arrest at G1/S stage, accompanied downregulation CDK4 Cyclin D1. Furthermore, significant elevation intracellular reactive oxygen species (ROS), mitochondrial ROS, DNA damage. Supplementation with antioxidant NAC effectively attenuated EOM-induced cardiac senescence. Our findings revealed activated aryl hydrocarbon receptor (AhR) signaling pathway, evidenced AhR translocation nucleus upregulation Cyp1a1 Cyp1b1. Importantly, antagonist CH223191 mitigated oxidative stress conclusion, our results indicate PM2.5-induced activation leads stress, damage, arrest, leading Targeting AhR/ROS axis might be promising therapeutic strategy for combating aging.

Language: Английский

Citations

7
Ambient particulate matter exposure induces ferroptosis in hippocampal cells through the GSK3B/Nrf2/GPX4 pathway DOI
Jianxiong Gui, Lingman Wang, Jie Liu

et al.

Free Radical Biology and Medicine, Journal Year: 2024, Volume and Issue: 213, P. 359 - 370

Published: Jan. 28, 2024

Language: Английский

Citations

6