Molecular Medicine, Год журнала: 2024, Номер 30(1)
Опубликована: Дек. 20, 2024
Язык: Английский
Frontiers in Pharmacology, Год журнала: 2023, Номер 14
Опубликована: Июнь 27, 2023
Aging is an inevitable process influenced by genetics, lifestyles, and environments. With the rapid social economic development in recent decades, proportion of elderly has increased rapidly worldwide, many aging-related diseases have shown upward trend, including nervous system diseases, cardiovascular metabolic cancer. The rising burden become urgent global health challenge requires immediate attention solutions. Natural products been used for a long time to treat various human diseases. primary cellular pathways that mediate longevity-extending effects natural involve nutrient-sensing pathways. Among them, sirtuin, AMP-activated protein kinase, mammalian target rapamycin, p53, insulin/insulin-like growth factor-1 signaling are most widely studied. Several studies reviewed individual compounds on aging along with underlying mechanisms. from food sources, such as polyphenols, saponins, alkaloids, polysaccharides, classified antiaging promote prolong life via In this article, we several recently identified potential properties highlighted their molecular discovery use dietary supplements can prevent multiple humans will be beneficial. Thus, review provides theoretical background existing agents.
Язык: Английский
Процитировано
32
Food Bioscience, Год журнала: 2024, Номер 61, С. 104695 - 104695
Опубликована: Июль 4, 2024
Язык: Английский
Процитировано
5
Human Genetics, Год журнала: 2025, Номер unknown
Опубликована: Янв. 8, 2025
Refractive error (RE) and myopia are complex polygenic conditions with the majority of genome-wide associated genetic variants in non-exonic regions. Given this, onset during childhood, gene-regulation is expected to play an important role its pathogenesis. This prompted us explore beyond traditional gene finding approaches. We performed a association study between non-coding RNAs enhancers, RE myopia. obtained single-nucleotide polymorphisms (SNPs) microRNA (miRNA) genes, miRNA-binding sites, long genes (lncRNAs) enhancers from publicly available databases: miRNASNPv2, PolymiRTS, VISTA Enhancer Browser, FANTOM5 lncRNASNP2. investigated whether SNPs overlapping these elements were leveraged large GWAS meta-analysis (N = 160,420). With risk scores (GRSs) per element, we joint effect on RE, axial length (AL)/corneal radius (CR), AL progression independent child cohort, Generation R Study 3638 children). constructed score for biological plausibility SNP highly confident sites chromatin accessible found that two miRNA 14 81 lncRNA regions 54 myopia-associated loci. GRSs significantly AL/CR progression. lncRNAs all miRNAs not any ocular biometric measurement. showed suggestive but inconsistent significance. prioritized candidate binding future functional validation. Pathways target host ranked included eye development (BMP4, MPPED2), neurogenesis (DDIT4, NTM), extracellular matrix (ANTXR2, BMP3), photoreceptor metabolism (DNAJB12), morphogenesis (CHDR1), neural signaling (VIPR2) TGF-beta (ANAPC16). first large-scale Enhancers could be importance as they childhood provide blueprint validation by prioritizing enhancers.
Язык: Английский
Процитировано
0
Survey of Ophthalmology, Год журнала: 2025, Номер unknown
Опубликована: Март 1, 2025
Язык: Английский
Процитировано
0
Food Bioscience, Год журнала: 2023, Номер 56, С. 103322 - 103322
Опубликована: Ноя. 2, 2023
Язык: Английский
Процитировано
8
Journal of Translational Medicine, Год журнала: 2023, Номер 21(1)
Опубликована: Июнь 20, 2023
Although the executive pathways of senescence are known, underlying control mechanisms diverse and not fully understood, particularly how cancer cells avoid triggering despite experiencing exacerbated stress conditions within tumor microenvironment.Mass spectrometry (MS)-based proteomic screening was used to identify differentially regulated genes in serum-starved hepatocellular carcinoma RNAi employed determine knockdown phenotypes prioritized genes. Thereafter, gene function investigated using cell proliferation assays (colony-formation, CCK-8, Edu incorporation cycle) together with cellular (SA-β-gal, SAHF SASP). Gene overexpression techniques were applied examine mRNA protein regulation combination luciferase reporter proteasome degradation assays, respectively. Flow cytometry detect changes reactive oxygen species (ROS) vivo examined a xenograft model.Among induced by serum deprivation, NIPSNAP1 selected for investigation. Subsequent experiments revealed that promotes inhibits P27-dependent induction via dual mechanisms. Firstly, maintains levels c-Myc sequestering E3 ubiquitin ligase FBXL14 prevent proteasome-mediated turnover c-Myc. Intriguingly, restrained transcriptional repression mediated c-Myc-Miz1, lifted response withdrawal, thus identifying feedback between Secondly, shown modulate ROS promoting interactions deacetylase SIRT3 superoxide dismutase 2 (SOD2). Consequent activation SOD2 serves maintain below critical required induce cycle arrest senescence. Importantly, actions preventing recapitulated models.Together, these findings reveal as an important mediator negative regulator These also provide theoretical basis therapy where targeting invokes
Язык: Английский
Процитировано
7
International Journal of Molecular Sciences, Год журнала: 2023, Номер 24(14), С. 11554 - 11554
Опубликована: Июль 17, 2023
Ninjurin 1 (NINJ1) is a double-transmembrane cell-surface protein that might mediate plasma membrane rupture (PMR) and the diffusion of inflammatory factors. PMR characteristic acinar cell injury in severe acute pancreatitis (SAP). However, involvement NINJ1 mediating cells SAP currently unclear. Our study has shown expressed cells, expression significantly upregulated sodium-taurocholate-induced SAP. The knockout delays alleviates Moreover, we observed mediated by Ca2+ concentration cells. Importantly, found overload drives mitochondrial stress to upregulate P53/NINJ1 pathway, inducing amlodipine, channel inhibitor, can reduce occurrence decreasing Ca2+. results demonstrate mechanism which induces provide potential new target for treatment
Язык: Английский
Процитировано
7
The FASEB Journal, Год журнала: 2023, Номер 37(10)
Опубликована: Сен. 28, 2023
Brain aging is the most important risk factor for neurodegenerative disorders, and abnormal apoptosis linked to neuronal dysfunction. Specifically, studies have found that exercise effectively inhibits hippocampal apoptosis, while molecular mechanism remains unclear. In present study, we investigated impact of aerobic on in mice potential involvement DAPK1 its downstream pathways based recent data may be associated with death diseases. Senescent were subjected 8 weeks Aerobic training. Following behavioral testing, samples examined histologically biochemically detect pathological changes, mRNA protein levels. We intervention improved spatial memory alleviated brain. Notably, down-regulated expression inhibited Fas receptor transactivation mitochondrial apoptotic pathway hippocampus. These results shed new light protective effect regular against brain though modulating pathway.
Язык: Английский
Процитировано
7
AJP Cell Physiology, Год журнала: 2023, Номер 326(2), С. C386 - C399
Опубликована: Дек. 18, 2023
Nucleus pulposus cell (NPC) senescence is a major cause of intervertebral disc degeneration (IVDD). Oxidative stress and reactive oxygen species (ROS) play critical roles in regulating senescence. Selenophosphate synthetase 1 (SEPHS1) was reported to an important role mitigating oxidative osteoarthritis (OA) model by reducing the production ROS, thereby, delaying occurrence development osteoarthritis. In this study, we explored the, hitherto unknown, SEPHS1 IVDD vitro vivo using interleukin-1β (IL-1β)-induced NPC rat needle puncture model, respectively. delayed ROS production. Age-related dysfunction also ameliorated overexpression inhibition Hippo-Yap/Taz signaling pathway. experiments revealed that alleviated rats. Moreover, selenium (Se)-deficient diet lack synergistically aggravated progression. Taken together, our results demonstrate plays significant Overexpression can delay senescence, restore balance extracellular matrix metabolism, attenuate IVDD. could be promising therapeutic target for
Язык: Английский
Процитировано
6
Environmental Toxicology, Год журнала: 2024, Номер unknown
Опубликована: Сен. 13, 2024
ABSTRACT Age‐related macular degeneration (AMD), a leading cause of blindness, is characterized by mitochondrial dysfunction retinal pigment epithelium (RPE) cells. EUK‐134 mimetic SOD2 and catalase, widely used for its antioxidant properties in models light‐induced damage or oxidative stress. However, effects on the retina are not yet clear. Here, we investigated capability averting AMD using sodium iodate (NaIO 3 )‐induced Balb/c mouse ARPE‐19 cells (adult RPE cell line). In vivo, effectively antagonized NaIO ‐induced deformation prevented outer inner nuclear layer thinning. addition, it was found that EUK‐134‐treated group significantly down‐regulated expression cleaved caspase‐3 compared with treated alone. Our results notably improved viability preventing ROS accumulation‐induced membrane potential depolarization‐mediated apoptosis ‐inducted Furthermore, could inhibit p‐ERK, p‐p38, p‐JNK, p‐p53, Bax, caspase‐9, caspase‐3, PARP increasing Bcl‐2 protein expression. Additionally, employed MAPK pathway inhibitors SB203580 (a p38 inhibitor), U0126 (an ERK SP600125 JNK inhibitor) to corroborate aforementioned observation. The support may prevent stress‐mediated retinopathy.
Язык: Английский
Процитировано
2