Ferroptosis as a Potential Therapeutic Target for Reducing Inflammation and Corneal Scarring in Bacterial Keratitis DOI Creative Commons
Qiankun Chen, Leying Wang, Yuan Wei

и другие.

Investigative Ophthalmology & Visual Science, Год журнала: 2024, Номер 65(2), С. 29 - 29

Опубликована: Фев. 21, 2024

Purpose: Bacterial keratitis (BK) is a serious ocular infection that can cause severe inflammation and corneal scarring, leading to vision loss. In this study, we aimed investigate the involvement of ferroptosis in pathogenesis BK. Methods: Transcriptome analysis was performed evaluate ferroptosis-related gene expression human BK corneas. Subsequently, mouse models Pseudomonas aeruginosa stromal stem cells (CSSCs) were validated. The mice treated with levofloxacin (LEV) or combined ferrostatin-1 (LEV+Fer-1). CSSCs lipopolysaccharide (LPS) LPS Fer-1. Inflammatory cytokines, α-SMA, regulators evaluated by RT-qPCR, immunostaining, Western blot. Iron reactive oxygen species (ROS) measured. Results: revealed significant alterations genes models, group LEV+Fer-1 exhibited reduced inflammatory cytokines (MPO, TNF-α, IFN-γ), decreased scarring α-SMA expression, lower Fe3+ compared LEV groups. Notably, showed elevated GPX4 SLC7A11 contrast group. vitro, Fer-1 treatment effectively restored ROS, Fe2+, GPX4, induced CSSCs. Conclusions: Ferroptosis plays crucial role inhibition holds promise for mitigating inflammation, reducing ultimately enhancing prognosis Consequently, study provides potential target innovative therapeutic strategies BK, which immense transform

Язык: Английский

Ferroptosis contributes to endometrial fibrosis in intrauterine adhesions DOI
Qi Zhu, Simin Yao,

Ziying Ye

и другие.

Free Radical Biology and Medicine, Год журнала: 2023, Номер 205, С. 151 - 162

Опубликована: Июнь 10, 2023

Язык: Английский

Процитировано

20

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

Yu Ren,

Liyun Song

и другие.

Biomedicine & Pharmacotherapy, Год журнала: 2024, Номер 172, С. 116270 - 116270

Опубликована: Фев. 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

Язык: Английский

Процитировано

9

Ferroptosis in Glaucoma: A Promising Avenue for Therapy DOI
Jingyun Zhu, Hui Chen, Jian Wu

и другие.

Advanced Biology, Год журнала: 2024, Номер 8(5)

Опубликована: Фев. 27, 2024

Abstract Glaucoma, a blind‐leading disease largely since chronic pathological intraocular high pressure (ph‐IOP). Hitherto, it is reckoned incurable for irreversible neural damage and challenges in managing IOP. Thus, significant to develop neuroprotective strategies. Ferroptosis, initially identified as an iron‐dependent regulated death that triggers Fenton reactions culminates lipid peroxidation (LPO), has emerged focal point multiple tumors neurodegenerative diseases. Researches show iron homeostasis play critical roles the optic nerve (ON) retinal ganglion cells (RGCs), suggesting targeted treatments could be effective. In glaucoma, apart from lesions, disrupted metal balance increased oxidative stress trabecular meshwork (TM) are observed. These disturbances lead extracellular matrix excretion disorders, known sclerotic mechanisms, resulting refractory blockages. Importantly, stress, downstream effect of ferroptosis, also key factor cell senescence. It plays crucial role both etiology risk glaucoma. Moreover, ferroptosis induces non‐infectious inflammation, which exacerbate glaucomatous injury. Therefore, relevance glaucoma extensive multifaceted. this review, study delves into current understanding mechanisms aiming provide clues inform clinical therapeutic practices.

Язык: Английский

Процитировано

9

Ferrostatin-1 inhibits fibroblast fibrosis in keloid by inhibiting ferroptosis DOI Creative Commons
Yang Liu,

Xiuli Li,

Yanli Wang

и другие.

PeerJ, Год журнала: 2024, Номер 12, С. e17551 - e17551

Опубликована: Июнь 14, 2024

Background Keloid is a chronic proliferative fibrotic disease caused by abnormal fibroblasts proliferation and excessive extracellular matrix (ECM) production. Numerous disorders are significantly influenced ferroptosis, targeting ferroptosis can effectively mitigate fibrosis development. This study aimed to investigate the role mechanism of in keloid Methods tissues from patients normal skin healthy controls were collected. Iron content, lipid peroxidation (LPO) level, mRNA protein expression ferroptosis-related genes including solute carrier family 7 member 11 (SLC7A11), glutathione peroxidase 4 (GPX4), transferrin receptor (TFRC), nuclear factor erythroid 2-related 2 (Nrf2) determined. Mitochondrial morphology was observed using transmission electron microscopy (TEM). (KFs) isolated tissues, treated with inhibitor ferrostatin-1 (fer-1) or activator erastin. marker levels, LPO mitochondrial membrane potential, ATP KFs detected. Furthermore, levels α-smooth muscle actin (α-SMA), collagen I, III measured whether affect KFs. Results We found that iron content level substantially elevated SLC7A11, GPX4, Nrf2 downregulated TFRC upregulated Mitochondria exhibited pathology. Fer-1 treatment reduced restrained dysfunction KFs, Moreover, α-SMA, Whereas erastin showed opposite results. Conclusion Ferroptosis exists keloid. Ferrostatin-1 ECM deposition through inhibiting induced intensifying ferroptosis.

Язык: Английский

Процитировано

9

Ferroptosis as a Potential Therapeutic Target for Reducing Inflammation and Corneal Scarring in Bacterial Keratitis DOI Creative Commons
Qiankun Chen, Leying Wang, Yuan Wei

и другие.

Investigative Ophthalmology & Visual Science, Год журнала: 2024, Номер 65(2), С. 29 - 29

Опубликована: Фев. 21, 2024

Purpose: Bacterial keratitis (BK) is a serious ocular infection that can cause severe inflammation and corneal scarring, leading to vision loss. In this study, we aimed investigate the involvement of ferroptosis in pathogenesis BK. Methods: Transcriptome analysis was performed evaluate ferroptosis-related gene expression human BK corneas. Subsequently, mouse models Pseudomonas aeruginosa stromal stem cells (CSSCs) were validated. The mice treated with levofloxacin (LEV) or combined ferrostatin-1 (LEV+Fer-1). CSSCs lipopolysaccharide (LPS) LPS Fer-1. Inflammatory cytokines, α-SMA, regulators evaluated by RT-qPCR, immunostaining, Western blot. Iron reactive oxygen species (ROS) measured. Results: revealed significant alterations genes models, group LEV+Fer-1 exhibited reduced inflammatory cytokines (MPO, TNF-α, IFN-γ), decreased scarring α-SMA expression, lower Fe3+ compared LEV groups. Notably, showed elevated GPX4 SLC7A11 contrast group. vitro, Fer-1 treatment effectively restored ROS, Fe2+, GPX4, induced CSSCs. Conclusions: Ferroptosis plays crucial role inhibition holds promise for mitigating inflammation, reducing ultimately enhancing prognosis Consequently, study provides potential target innovative therapeutic strategies BK, which immense transform

Язык: Английский

Процитировано

8