Viral Infections and the Glutathione Peroxidase Family: Mechanisms of Disease Development DOI
Qingqing Lu, Yuan Ding, Wen Liu

et al.

Antioxidants and Redox Signaling, Journal Year: 2024, Volume and Issue: unknown

Published: Oct. 24, 2024

The glutathione peroxidase (GPx) family is recognized for its essential function in maintaining cellular redox balance and countering the overproduction of reactive oxygen species (ROS), a process intricately linked to progression various diseases including those spurred by viral infections. modulation GPx activity viruses presents critical juncture disease pathogenesis, influencing responses trajectory infection-induced diseases.

Language: Английский

Targeting PIM1 by Bruceine D attenuates skin fibrosis via myofibroblast ferroptosis DOI Creative Commons

Jianzhang Wang,

Yajuan Song,

Xiao-Ying Tan

et al.

Redox Biology, Journal Year: 2025, Volume and Issue: unknown, P. 103619 - 103619

Published: March 1, 2025

Language: Английский

Citations

0
Double-edged sword effect of GPX4 in skin homeostasis and diseases DOI
Hanzhang Xu, Yang Li, Yingli Wu

et al.

Archives of Dermatological Research, Journal Year: 2025, Volume and Issue: 317(1)

Published: Feb. 14, 2025

Language: Английский

Citations

0
Increased melanin induces aberrant keratinocyte − melanocyte − basal − fibroblast cell communication and fibrogenesis by inducing iron overload and ferroptosis resistance in keloids DOI Creative Commons
Xiangguang Shi,

Xueyi Xia,

Yang Xiao

et al.

Cell Communication and Signaling, Journal Year: 2025, Volume and Issue: 23(1)

Published: March 18, 2025

Keloid is a typical skin fibrotic disease with unclear mechanisms and limited therapeutic options. Fibroblast-induced fibrogenesis crucial cause of KD. However, the types cells involved in fibroblast KD specific are unclear. This study aimed to investigate role melanocyte-secreted melanin promoting its mechanism evaluate potential effect intervening treating keloid. The activity pigmentation-related pathways melanocytes was examined using single-cell RNA-sequence (scRNA-seq) analysis. Masson-Fontana staining or isolated quantification detected levels distribution cells. Collagen deposition, wounding healing, proliferation analysis were employed integratively assess fibrogenesis. After treatment, bulk-seq identified fibroblasts' differentially expressed genes (DEGs). iron by Perl's quantification. Cell viability, LipidROS, malondialdehyde assay accessed ferroptosis levels. ML329 evaluated keloid-bearing mice. We found enriched keloid further validated increased patients. Additionally, positively correlated Area Severity Index Furthermore, significantly promoted proliferation, migration, collagen synthesis. Mechanically, basal cell permeability inflammation facilitate transfer dermis, where it activated fibroblasts evoking overload resistance. Consistently, resistance primary tissues Inhibition effectively diminish melanin-induced Interestingly, induced an autocrine manner stimulated keratinocytes take up deepen color upregulating F2R-like trypsin receptor 1 (F2RL1). In vivo, delivery ML329, microphthalmia-associated transcription factor (MITF) inhibitor, could suppress melanogenesis alleviate human nude Meanwhile, decreased content restored sensitivities ferroptosis. Collectively, melanin-lowing strategies may appear as new target for Current treatments ineffective. Our research demonstrates that increase patients play significant progression mediating aberrant keratinocyte − melanocyte crosstalk. Importantly, we pharmacological inhibition MITF shows promise alleviating keloid, offering breakthrough treatment. synthesis pathway abnormally melanocytes. Melanin destroys membrane barrier triggering translocates dermal layers paracrine induce overgrowth, ECM deposition inducing maintains melanocytes' hyperproliferative non-immortal properties manner. It enhances keratocyte PAR-2 promote transit superficial epidermis layers, which be related deepening color. alleviates

Language: Английский

Citations

0
Skin Aging and the Upcoming Role of Ferroptosis in Geroscience DOI Open Access
Rita Rezzani, Gaia Favero,

Giorgia Cominelli

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(15), P. 8238 - 8238

Published: July 28, 2024

The skin is considered the most important organ system in mammals, and as population ages, it to consider aging anti-aging therapeutic strategies. Exposure of various insults induces significant changes throughout our lives, differentiating a young adult from that an older adult. These are caused by combination intrinsic extrinsic aging. We report interactions between its metabolism, showing network due several factors. For example, iron nutrient for humans, but level increases with aging, inducing deleterious effects on cellular functions. Recently, was discovered ferroptosis, or iron-dependent cell death, linked diseases. pursuit new molecular targets ferroptosis has recently attracted attention. Prevention effective strategy treatment diseases, especially old age. However, pathological biological mechanisms underlying still not fully understood, diseases such melanoma autoimmune Only few basic studies regulated death exist, challenge turn into clinical applications.

Language: Английский

Citations

1
Increased melanin induces aberrant keratinocyte−melanocyte−basal−fibroblast cell communication and fibrogenesis by inducing iron overload and ferroptosis resistance in keloids DOI Creative Commons
Xiangguang Shi,

Xueyi Xia,

Yang Xiao

et al.

Research Square (Research Square), Journal Year: 2024, Volume and Issue: unknown

Published: Nov. 15, 2024

Abstract Keloid is a typical skin fibrotic disease with unclear mechanisms and limited therapeutic options. In this study, we found the enriched pigmentation-related pathways in melanocytes of keloid by single-cell RNA-sequence (scRNA-seq) analysis. We further validated increased melanin levels patients. Additionally, positively correlated Area Severity Index keloid. Furthermore, melanocyte-secreted significantly promoted fibroblast proliferation, migration, collagen synthesis. Mechanically, basal cell permeability inflammation to facilitate its transfer dermis, where it activated fibroblasts evoking iron overload ferroptosis resistance. Consistently, resistance were primary tissues Inhibition effectively diminish melanin-induced fibrogenesis. Interestingly, induced an autocrine manner stimulated keratinocytes take up deepen color upregulating F2R-like trypsin receptor 1 (F2RL1). In vivo, delivery ML329, micropthalmia-associated transcription factor (MITF) inhibitor, could suppress melanogenesis alleviate human keloid-bearing nude mice. Meanwhile, ML329 decreased content restored sensitivities ferroptosis. Collectively, melanin-lowing strategies may appear as potential new target for

Language: Английский

Citations

1
Viral Infections and the Glutathione Peroxidase Family: Mechanisms of Disease Development DOI
Qingqing Lu, Yuan Ding, Wen Liu

et al.

Antioxidants and Redox Signaling, Journal Year: 2024, Volume and Issue: unknown

Published: Oct. 24, 2024

The glutathione peroxidase (GPx) family is recognized for its essential function in maintaining cellular redox balance and countering the overproduction of reactive oxygen species (ROS), a process intricately linked to progression various diseases including those spurred by viral infections. modulation GPx activity viruses presents critical juncture disease pathogenesis, influencing responses trajectory infection-induced diseases.

Language: Английский

Citations

0