Targeting Nano-Proanthocyanidins Alleviate Silicosis Fibrosis by Improving the Cross-Talk between Macrophage and Fibroblasts DOI
Yue Sun, Mengxue Yu,

Sirong Chang

et al.

Published: Jan. 1, 2024

AbstractSilicosis is one of the most common and rapidly progressing occupational diseases in world, there still no specific drug to reverse end-stage diffuse interstitial fibrosis. Strikingly, crosstalk between macrophages fibroblasts plays a vital role development silicosis Here we study nano-miniaturization natural compounds, proanthocyanidins, alleviate via mediating interaction above cells. In this study, proanthocyanidins were loaded into mesoporous Prussian blue coated by hyaluronic acid-inserted macrophage membrane, termed as HMP@PC NPs. vitro, macrophages-targeted NPs inhibits activation blunting M1/M2 polarization accordingly inflammatory cytokines co-culture system. vivo, safety not only alleviates SiO2-induced fibrosis, but also remodel benign intestinal microbiota homeostasis corresponding non-targeted metabolites. These findings could benefit for potential therapeutic strategy treat

Language: Английский

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

3
Advances in Ferroptosis Research: A Comprehensive Review of Mechanism Exploration, Drug Development, and Disease Treatment DOI Creative Commons
Haojie Wang, Yuanyuan Xie

Pharmaceuticals, Journal Year: 2025, Volume and Issue: 18(3), P. 334 - 334

Published: Feb. 26, 2025

In recent years, ferroptosis, as an emerging modality of programmed cell death, has captured significant attention within the scientific community. This comprehensive review meticulously canvasses pertinent literature past few spanning multiple facets. It delves into intricate mechanisms underpinning tracks evolution its inducers and inhibitors, dissects roles in a diverse array diseases, well resultant therapeutic implications. A profound exploration is conducted functional ferroptosis-related molecules, intracellular pathways, metabolic cascades, signaling transduction routes. Novel ferroptosis inhibitors are introduced detail, covering their design blueprints, synthetic methodologies, bioactivity profiles. Moreover, exhaustive account provided regarding involvement malignancies, neurodegenerative disorders, cardiovascular ailments, other pathologies. By highlighting pivotal status potential regimens various this aspires to furnish thorough reference framework for future investigations clinical translations domain.

Language: Английский

Citations

2
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

9
Important molecular mechanisms in ferroptosis DOI

Lunmeng Lai,

Menglei Tan,

Mingming Hu

et al.

Molecular and Cellular Biochemistry, Journal Year: 2024, Volume and Issue: unknown

Published: April 26, 2024

Language: Английский

Citations

6
A Multifunctional Nanocomposite Hydrogel Delivery System Based on Dual‐Loaded Liposomes for Scarless Wound Healing DOI
Danlei Xing,

Guoqing Xia,

Xu-Dong Tang

et al.

Advanced Healthcare Materials, Journal Year: 2024, Volume and Issue: 13(28)

Published: July 16, 2024

Abstract Increased inflammatory responses and oxidative stress at the wound site following skin trauma impair healing. Furthermore, scarring places fibroblasts under severe mechanical aggravates pathological fibrosis. A novel liposomal composite hydrogel is engineered for microenvironment remodeling, incorporating dual‐loaded liposomes into gelatin methacrylate to create a nanocomposite hydrogel. Notably, tetrahydrocurcumin (THC) hepatocyte growth factor (HGF) are encapsulated in hydrophobic hydrophilic layers of liposomes, respectively. The maintains porous nanoarchitecture, demonstrating sustainable THC HGF release enhanced properties biocompatibility. This system effectively promotes cell proliferation angiogenesis attenuates apoptosis. It decreases expression factors by inhibiting high‐mobility group box /receptor advanced glycation end product/NF‐κB (HMGB1/RAGE/NF‐κB)pathway increases macrophage polarization from M1 M2 vitro, controlling responses. exhibits remarkable antioxidant scavenging excess reactive oxygen species free radicals. Most importantly, it prevents scar formation restraining transforming beta (TGF‐β)/Smads pathway that downregulates associated fibrotic factors. demonstrates strong therapeutic effects against inflammation fibrosis rat model with biosafety, advancing development innovative hydrogel‐based delivery strategies clinical scarless therapy.

Language: Английский

Citations

6
Analyzing how SiMiao Wan regulates ferroptosis to prevent RA-ILD using metabolomics and cyberpharmacology DOI

Yanhua Chen,

huimin Liu,

Rui Han

et al.

Phytomedicine, Journal Year: 2024, Volume and Issue: 133, P. 155912 - 155912

Published: July 22, 2024

Language: Английский

Citations

5
RELA-mediated upregulation of LINC03047 promotes ferroptosis in silica-induced pulmonary fibrosis via SLC39A14 DOI
Binbin Zhang, Enze Wang,

Sijing Zhou

et al.

Free Radical Biology and Medicine, Journal Year: 2024, Volume and Issue: 223, P. 250 - 262

Published: Aug. 5, 2024

Language: Английский

Citations

4
Pulmonary fibrosis: pathogenesis and therapeutic strategies DOI Creative Commons
Jianhai Wang, Kuan Li,

De Hao

et al.

MedComm, Journal Year: 2024, Volume and Issue: 5(10)

Published: Sept. 23, 2024

Abstract Pulmonary fibrosis (PF) is a chronic and progressive lung disease characterized by extensive alterations of cellular fate function excessive accumulation extracellular matrix, leading to tissue scarring impaired respiratory function. Although our understanding its pathogenesis has increased, effective treatments remain scarce, fibrotic progression major cause mortality. Recent research identified various etiological factors, including genetic predispositions, environmental exposures, lifestyle which contribute the onset PF. Nonetheless, precise mechanisms these factors interact drive are not yet fully elucidated. This review thoroughly examines diverse molecular mechanisms, key signaling pathways involved in PF, such as TGF‐β, WNT/β‐catenin, PI3K/Akt/mTOR. It also discusses current therapeutic strategies, antifibrotic agents like pirfenidone nintedanib, explores emerging targeting senescence. Emphasizing need for omni‐target approaches overcome limitations therapies, this integrates recent findings enhance PF development more prevention management ultimately improving patient outcomes.

Language: Английский

Citations

4
Targeting progranulin alleviated silica particles-induced pulmonary inflammation and fibrosis via decreasing Il-6 and Tgf-β1/Smad DOI

Manyu Zhao,

Mengzhu Wang, Xuxi Chen

et al.

Journal of Hazardous Materials, Journal Year: 2023, Volume and Issue: 465, P. 133199 - 133199

Published: Dec. 10, 2023

Language: Английский

Citations

10
Role of environmental pollutants-induced ferroptosis in pulmonary diseases DOI Creative Commons
Long Yang, Yuan Qiao, Zeyu Huang

et al.

Frontiers in Medicine, Journal Year: 2025, Volume and Issue: 12

Published: Feb. 24, 2025

Respiratory diseases rank among the foremost causes of mortality and disability globally, with long-term exposure to environmental pollutants playing a critical role in their onset progression. Despite this, underlying mechanisms effective targeted treatments for these disorders remain poorly understood, highlighting an urgent need focused research. Cell death, programmed cellular response external harmful stimuli, including ferroptosis-a recently identified form iron-dependent cell death-emerges as pivotal process. Characterized by intracellular iron accumulation lipid peroxidation, ferroptosis appears intricately linked lung injury induced pollutants. This review examines triggered factors, aiming shed light on its specific pathophysiological potential therapeutic target. By deepening our understanding interactions between pollution, ferroptosis, damage, we hope inform strategies intervention.

Language: Английский

Citations

0