The multiple biological activities of hyperoside: from molecular mechanisms to therapeutic perspectives in neoplastic and non-neoplastic diseases DOI Creative Commons

Weisong Zhang,

Rui Wang, Rongqi Guo

и другие.

Frontiers in Pharmacology, Год журнала: 2025, Номер 16

Опубликована: Март 3, 2025

In recent years, hyperoside (quercetin 3-O-β-D-galactopyranoside) has garnered significant attention due to its diverse biological effects, which include vasoprotective, antioxidant, anti-inflammatory, and anti-tumor properties. Notably, shown remarkable potential in cancer therapy by targeting multiple mechanisms; it induces apoptosis, inhibits proliferation, blocks angiogenesis, reduces the metastatic of cells. Furthermore, enhances sensitivity cells chemotherapy modulating key signaling pathways. Beyond neoplastic diseases, also presents promising therapeutic applications managing non-cancerous conditions such as diabetes, Alzheimer’s disease, pulmonary fibrosis. This review comprehensively examines molecular mechanisms underlying hyperoside’s anti-cancer effects highlights role treatment cancers, including lung colorectal cancers. Additionally, explores latest research on addressing non-neoplastic conditions, fibrosis, Parkinson’s disease. By summarizing current findings, this underscores unique value a multifunctional both contexts.

Язык: Английский

Microplastic and plastic pollution: impact on respiratory disease and health DOI Creative Commons
Gwenda F. Vasse, Barbro N. Melgert

European Respiratory Review, Год журнала: 2024, Номер 33(172), С. 230226 - 230226

Опубликована: Апрель 30, 2024

Throughout their lifecycle, from production to use and upon disposal, plastics release chemicals particles known as micro- nanoplastics (MNPs) that can accumulate in the environment. MNPs have been detected different locations of human body, including our lungs. This is likely a consequence MNP exposure through air we breathe. Yet, still lack comprehensive understanding impact may on respiratory disease health. In this review, collated current body evidence implications inhalation lung health vitro , vivo occupational studies. We focused interactions between pollution specific lung-resident cells diseases. conclude it evident possess capacity affect tissue remains unclear which extent occurs ambient levels MNPs, emphasising need for more evaluation environmental everyday life.

Язык: Английский

Процитировано

30
Ferroptosis in Pulmonary Disease and Lung Cancer: Molecular Mechanisms, Crosstalk Regulation, and Therapeutic Strategies DOI Creative Commons
Dandan Guo, Songhua Cai,

Lvdan Deng

и другие.

MedComm, Год журнала: 2025, Номер 6(3)

Опубликована: Фев. 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.

Язык: Английский

Процитировано

3
Emerging roles of ferroptosis in pulmonary fibrosis: current perspectives, opportunities and challenges DOI Creative Commons
Yixiang Hu,

Ying Huang,

Lijuan Zong

и другие.

Cell Death Discovery, Год журнала: 2024, Номер 10(1)

Опубликована: Июнь 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.

Язык: Английский

Процитировано

11
Engineering Lipid Nanoparticles to Enhance Intracellular Delivery of Transforming Growth Factor-Beta siRNA (siTGF-β1) via Inhalation for Improving Pulmonary Fibrosis Post-Bleomycin Challenge DOI Creative Commons
Xu Deng,

Yingjie Yang,

Li‐Ming Gan

и другие.

Pharmaceutics, Год журнала: 2025, Номер 17(2), С. 157 - 157

Опубликована: Янв. 24, 2025

Background/Objectives: Transforming Growth Factor-beta (TGFβ1) plays a core role in the process of pulmonary fibrosis (PF). The progression can be alleviated by siRNA-based inhibiting TGF-β1. However, limitations naked siRNA lead to failure achieving therapeutic effect. This study aimed design lipid nanoparticles (LNPs) that deliver siTGF-β1 lungs for purposes. Methods: cytotoxicity and transfection assay vitro were used screen ionizable lipids (ILs). Design Experiments (DOE) was obtain novel LNPs enhance resistance atomization shear forces. Meanwhile, impact encapsulating (siTGFβ1-LNPs) on PF investigated. Results: When DLin-DMA-MC3 (MC3) as ILs, phase ratio MC3:DSPC:DMG-PEG2000:cholesterol = 50:10:3:37, N/P 3.25; siTGFβ1-LNPs could stably delivered via converting solution into an aerosol (atomization). In experiments have confirmed high safety, encapsulation, promote cellular uptake endosomal escape. addition, significantly reduced inflammatory infiltration attenuated deposition extracellular matrix (ECM) protected lung tissue from toxicity bleomycin (BLM) without causing systemic toxicity. Conclusions: effectively lungs, resulting silencing TGF-β1 mRNA inhibition epithelial–mesenchymal transition pathway, thereby delaying PF, which provides new method treatment intervention PF.

Язык: Английский

Процитировано

1
Molecular Mechanisms Responsible for the Therapeutic Potential of Mesenchymal Stem Cell-Derived Exosomes in the Treatment of Lung Fibrosis DOI Open Access
Carl Randall Harrell, Valentin Djonov, Ana Volarevic

и другие.

International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(8), С. 4378 - 4378

Опубликована: Апрель 16, 2024

Mesenchymal stem cell-derived exosomes (MSC-Exos) are nano-sized extracellular vesicles which contain various MSC-sourced anti-fibrotic, immunoregulatory and angio-modulatory proteins (growth factors, cytokines, chemokines), lipids, nucleic acids (messenger RNA microRNAs). Due to their lipid envelope, MSC-Exos easily by-pass all barriers in the body deliver cargo directly target cells, modulating viability, proliferation, phenotype function. The results obtained recently published experimental studies demonstrated beneficial effects of treatment lung fibrosis. reduced activation fibroblasts prevented differentiation myofibroblasts. By delivering factors lung-infiltrated monocytes T modulate function, alleviating on-going inflammation may also serve as vehicles for delivery anti-fibrotic immunomodulatory agents, enabling enhanced attenuation Although numerous pre-clinical have therapeutic potential pulmonary fibrosis, there several challenges that currently hinder clinical implementation. Therefore, this review article, we summarized current knowledge discussed future perspectives regarding molecular cellular mechanisms were responsible anti-inflammatory properties MSC-Exos, paving way use

Язык: Английский

Процитировано

7
Protein prenylation in mechanotransduction: implications for disease and therapy DOI
Heng Chen, Jian Yang,

Qingzhen Yang

и другие.

Trends in Pharmacological Sciences, Год журнала: 2025, Номер unknown

Опубликована: Янв. 1, 2025

Язык: Английский

Процитировано

1
LGALS3 regulates endothelial-to-mesenchymal transition via PI3K/AKT signaling pathway in silica-induced pulmonary fibrosis DOI

Demin Cheng,

Wenxiu Lian,

Xinying Jia

и другие.

Toxicology, Год журнала: 2024, Номер 509, С. 153962 - 153962

Опубликована: Сен. 29, 2024

Язык: Английский

Процитировано

6
NLRP3 inflammasome mediates abnormal epithelial regeneration and distal lung remodeling in silica‑induced lung fibrosis DOI Creative Commons

Hong Zhou,

Qun Zhang, Chenyang Liu

и другие.

International Journal of Molecular Medicine, Год журнала: 2024, Номер 53(3)

Опубликована: Янв. 16, 2024

NOD-like receptor protein 3 (NLRP3) inflammasome is closely related to silica particle‑induced chronic lung inflammation but its role in epithelial remodeling, repair and regeneration the distal during development of silicosis remains be elucidated. The present study aimed determine effects NLRP3 on remodeling cellular potential mechanisms silica‑treated mice at three time points. Pulmonary function assessment, inflammatory cell counting, enzyme‑linked immunosorbent assay, histological immunological analyses, hydroxyproline assay western blotting were used study. Single intratracheal instillation a suspension caused sustained activation lung. Moreover, time‑dependent increase airway resistance decrease compliance accompanied progression pulmonary fibrosis. In terminal bronchiole, including pyroptosis (membrane‑distributed GSDMD+), excessive proliferation (Ki67+), mucus overproduction (mucin 5 subtype AC B) epithelial‑mesenchymal transition (decreased E‑Cadherin+ increased Vimentin+), was observed by immunofluorescence analysis. Notably, aberrant spatiotemporal expression embryonic stem/progenitor markers SOX2 SOX9 ectopic distribution bronchioalveolar stem cells only 7th day after (the early phase silicosis). Western revealed that Sonic hedgehog/Glioma‑associated oncogene (Shh/Gli) Wnt/β‑catenin pathways involved activation‑mediated dysregulated fibrotic phases. Overall, led mice. understanding profile may provide novel therapeutic strategy for inhalable particle‑related disease.

Язык: Английский

Процитировано

5
GLP-1R activation attenuates the progression of pulmonary fibrosis via disrupting NLRP3 inflammasome/PFKFB3-driven glycolysis interaction and histone lactylation DOI Creative Commons
Chenyang Liu, Qun Zhang,

Hong Zhou

и другие.

Journal of Translational Medicine, Год журнала: 2024, Номер 22(1)

Опубликована: Окт. 21, 2024

Pulmonary fibrosis is a serious interstitial lung disease with no viable treatment except for transplantation. Glucagon-like peptide-1 receptor (GLP-1R), commonly regarded as an antidiabetic target, exerts antifibrotic effects on various types of organ fibrosis. However, whether GLP-1R modulates the development and progression pulmonary remains unclear. In this study, we investigated effect using in vitro vivo models A silica-induced mouse model was established to evaluate protective activating liraglutide vivo. Primary cultured fibroblasts treated TGF-β1 combined IL-1β (TGF-β1 + IL-1β) were used explore specific liraglutide, MCC950, 3PO fibroblast activation vitro. Cell metabolism assay performed determine glycolytic rate mitochondrial respiration. RNA sequencing utilized analyse underlying molecular mechanisms by which affects activation. ChIP‒qPCR histone lactylation at promoters profibrotic genes IL-1β- or exogenous lactate-stimulated fibroblasts. Activating attenuated inflammation mice exposed silica. Pharmacological inhibition NLRP3 inflammasome suppressed PFKFB3-driven glycolysis vice versa, resulting decreased lactate production IL-1β-stimulated inhibited IL-1β-induced disrupting interaction between subsequently prevented lactate-mediated reduce pro-fibrotic gene expression. addition, protected mitochondria against increase oxidative phosphorylation lactate-treated fibroblasts, not only repressed but also alleviated p300-mediated lactylation. Finally, blocked silica-treated macrophage-conditioned media-induced The could be attributed glycolysis, Thus, therapeutic target

Язык: Английский

Процитировано

5
Endothelial H2S-AMPK dysfunction upregulates the angiocrine factor PAI-1 and contributes to lung fibrosis DOI Creative Commons
Xiangqi Chen, Han Wang,

Chuan Wu

и другие.

Redox Biology, Год журнала: 2024, Номер 70, С. 103038 - 103038

Опубликована: Янв. 11, 2024

Dysfunction of the vascular angiocrine system is critically involved in regenerative defects and fibrosis injured organs. Previous studies have identified various factors found that risk such as aging metabolic disorders can disturb fibrotic One existing key gap what sense to modulate organ fibrosis. Here, using human mouse data, we discovered pathway hydrogen sulfide (H

Язык: Английский

Процитировано

5