Archives of Biochemistry and Biophysics, Journal Year: 2024, Volume and Issue: unknown, P. 110221 - 110221
Published: Nov. 1, 2024
Language: Английский
Frontiers in Cellular Neuroscience, Journal Year: 2024, Volume and Issue: 18
Published: March 7, 2024
Globally, millions of individuals are impacted by neurodegenerative disorders including Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), Parkinson's (PD), and Alzheimer's (AD). Although a great deal energy financial resources have been invested in disease-related research, breakthroughs therapeutic approaches remain elusive. The breakdown cells usually happens together with the onset diseases. However, mechanism that triggers neuronal loss is unknown. Lipid peroxidation, which iron-dependent, causes specific type cell death called ferroptosis, there evidence its involvement pathogenic cascade mechanisms still not well known. present article highlights basic processes underlie ferroptosis corresponding signaling networks. Furthermore, it provides an overview discussion current research on role across variety conditions.
Language: Английский
Citations
5
Cell Biology and Toxicology, Journal Year: 2024, Volume and Issue: 40(1)
Published: March 13, 2024
Abstract Intervertebral disc degeneration (IVDD) is an aging disease that results in a low quality of life and heavy socioeconomic burden. The mitochondrial unfolded protein response (UPR mt ) take part various aging-related diseases. Our research intents to explore the role underlying mechanism UPR IVDD. Nucleus pulposus (NP) cells were exposed IL-1β nicotinamide riboside (NR) served as inducer treat NP cells. Detection ATP, NAD + NADH used determine function mitochondria. MRI, Safranin O-fast green Immunohistochemical examination degree IVDD vivo. In this study, we discovered was increased markedly human tissues than healthy controls. vitro, mitophagy levels promoted treated with IL-1β. Upregulation by NR Atf5 overexpression inhibited cell apoptosis further improved mitophagy. Silencing Pink1 reversed protective effects induced . vivo, might attenuate IDD activating rats. summary, involved regulating Pink1-induced Mitophagy be latent target for Graphical • upregulated degenerative intervertebral disc. regulated could activate protect from apoptosis. Nicotinamide reduced apoptosis, thereby delaying process
Language: Английский
Citations
5
Journal of Agricultural and Food Chemistry, Journal Year: 2025, Volume and Issue: unknown
Published: March 12, 2025
Chronic exposure to arsenic (As), a ubiquitous contaminant, poses deleterious health risks humans, including cardiovascular disease. Recent studies have implicated ferroptosis, in which the essential micronutrient selenium (Se) plays crucial role, several As-induced pathological processes. However, whether Se can counteract endothelial dysfunction through ferroptosis remains unclear. Herein, methylseleninic acid (MSA), methylselenium metabolite, was used as supplement investigate underlying effect and mechanism of involving vivo vitro. As induced mice, indicated by increased aortic permeability, number circulating cells, mitochondria exhibiting ferroptosis-related alterations. Additionally, cell death mouse accompanied impaired redox homeostasis, relatively low status, decreased expressions selenoproteome, GPX4. Notably, these were attenuated MSA via activation Nrf2 upregulation three GPX4 isoforms, further abrogated antagonist ML385. Finally, exhibited ameliorative effects on aortas As-exposed mice. These results demonstrate that causes affecting Se-Nrf2/GPX4 axis, be relieved MSA. This study provides novel evidence implicating mitigating ferroptosis.
Language: Английский
Citations
0
Published: April 1, 2025
Language: Английский
Citations
0
Free Radical Biology and Medicine, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 1, 2025
Language: Английский
Citations
0
Frontiers in Pharmacology, Journal Year: 2025, Volume and Issue: 16
Published: Feb. 24, 2025
Atherosclerosis (AS)-related cardiovascular disease and depression are often comorbid, with patients facing an increased risk of depression, which worsens AS. Both diseases characterized by oxidative stress lipid metabolism disorders. Ferroptosis, a form cell death iron overload harmful peroxide accumulation, is found in various diseases, including AS depression. Consistent the deposition peroxidation (LPO) that characterize ferroptosis mechanism, disturbances also crucial pathogenic mechanisms The comorbid complex, posing challenges for clinical treatment. Chinese herbs hold significant potential owing to their multi-target pharmacological effects. Therefore, this review aims investigate overload, LPO, across types, shared pathogenesis ferroptosis, research on herbal medicine targeting treatment anti-AS co-depression. This provides comprehensive understanding co-depression from perspective ferroptosis.
Language: Английский
Citations
0
Journal of Cell Science, Journal Year: 2025, Volume and Issue: 138(6)
Published: March 15, 2025
ABSTRACT From border cell migration during Drosophila embryogenesis to solid stresses inside tumors, cells are often compressed physiological and pathological processes, triggering major responses. Cell compression can be observed in vivo but also controlled vitro through tools such as micro-channels or planar confinement assays. Such have recently become commercially available, allowing a broad research community tackle the role of variety contexts. This has led discovery conserved compression-triggered modes, fate determinants mechanosensitive pathways, among others. In this Review, we will first address different ways which their biological Then, discuss distinct mechanosensing mechanotransducing pathways that activate response compression. Finally, describe systems been engineered compress cells.
Language: Английский
Citations
0
Free Radical Biology and Medicine, Journal Year: 2025, Volume and Issue: unknown
Published: April 1, 2025
Language: Английский
Citations
0
Arthritis Research & Therapy, Journal Year: 2025, Volume and Issue: 27(1)
Published: April 17, 2025
Recently, several studies have reported that nucleus pulposus (NP) cell ferroptosis plays a key role in IDD. However, the characteristics and molecular mechanisms of subsets involved remain unclear. We aimed to define factors driving ferroptosis, ferroptotic NP cells during The accumulation iron ions tissues rats caudal intervertebral discs (IVDs) was determined by Prussian blue staining. Fluorescent probe Undecanoyl Boron Dipyrromethene (C11-BODIPY) lipid peroxidation product 4-Hydroxynonenal (4-HNE) staining were performed assess level cells. differentially expressed genes with aging overlapped FerrDB database screen associated aging-related In addition, single sequencing (ScRNA-seq) used map cells, further identify subsets, as well their crucial drivers. Finally, cluster analysis marker Histological showed that, compared 10 months old (10M-old) group, increased 20 (20M-old) rats, also enhanced. 15 related IDD selected cross-enrichment. ScRNA-seq identified 14 tissue among which number ratio 5 reduced, intracellular signaling pathways significantly enriched, accompanied enhanced peroxidation. Notably, ranking up-regulation fold genes, we found Atf3 always present within TOP2 these five suggests it is factor ferroptosis. cross-enrichment fluorescence colocalization revealed Rps6 +/Cxcl1- common feature subsets. This study reveals ATF3 driver IDD, These findings provide evidence theoretical support for subsequent targeted intervention directions preventing delaying
Language: Английский
Citations
0
Translational Oncology, Journal Year: 2025, Volume and Issue: 56, P. 102386 - 102386
Published: April 18, 2025
Language: Английский
Citations
0