Berberine promotes primordial follicle activation and increases ovulated oocyte quantity in aged mice DOI Creative Commons
Shuang Liu, Weiyong Wang, Huiyu Liu

et al.

Molecular Medicine, Journal Year: 2024, Volume and Issue: 30(1)

Published: Dec. 20, 2024

Language: Английский

Antiaging effects of dietary supplements and natural products DOI Creative Commons

Lulu Gao,

Xudong Liu, Xiaoyan Luo

et al.

Frontiers in Pharmacology, Journal Year: 2023, Volume and Issue: 14

Published: June 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.

Language: Английский

Citations

28

Protective effect of Cyanidin-3-O-glucoside from blueberry anthocyanin extracts against hyperglycemia-induced outer BRB damage by suppressing REDD1-mediated VEGFA upregulation DOI
Rui Li,

Shumeng Du,

Zhan Ye

et al.

Food Bioscience, Journal Year: 2024, Volume and Issue: 61, P. 104695 - 104695

Published: July 4, 2024

Language: Английский

Citations

4

A genome-wide scan of non-coding RNAs and enhancers for refractive error and myopia DOI Creative Commons
Milly S. Tedja, Joanna Swierkowska, Clair A. Enthoven

et al.

Human Genetics, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 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.

Language: Английский

Citations

0

The role of retinal pigment epithelial senescence and the potential of senotherapeutics in age-related macular degeneration DOI
Yingying Chen,

Feipeng Jiang,

Yue Zeng

et al.

Survey of Ophthalmology, Journal Year: 2025, Volume and Issue: unknown

Published: March 1, 2025

Language: Английский

Citations

0

Cyanidin-3-O-glucoside from blueberry anthocyanin extracts protects ARPE-19 cells against high glucose damage via REDD1/GSK3β pathway DOI
Rui Li, Zhan Ye, Yong‐Jiang Xu

et al.

Food Bioscience, Journal Year: 2023, Volume and Issue: 56, P. 103322 - 103322

Published: Nov. 2, 2023

Language: Английский

Citations

8

NIPSNAP1 directs dual mechanisms to restrain senescence in cancer cells DOI Creative Commons

Enyi Gao,

Xiaoya Sun, Rick F. Thorne

et al.

Journal of Translational Medicine, Journal Year: 2023, Volume and Issue: 21(1)

Published: June 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

Language: Английский

Citations

7

The Novel Application of EUK‐134 in Retinal Degeneration: Preventing Mitochondrial Oxidative Stress‐Triggered Retinal Pigment Epithelial Cell Apoptosis by Suppressing MAPK/p53 Signaling Pathway DOI

Shang‐Chun Tsou,

Chen‐Ju Chuang, Chin‐Lin Hsu

et al.

Environmental Toxicology, Journal Year: 2024, Volume and Issue: unknown

Published: Sept. 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.

Language: Английский

Citations

2

Deletion of the stress response protein REDD1 prevents sodium iodate-induced RPE damage and photoreceptor loss DOI Creative Commons
Sandeep Subrahmanian,

Esma I. Yerlikaya,

Siddharth Sunilkumar

et al.

GeroScience, Journal Year: 2024, Volume and Issue: unknown

Published: Oct. 5, 2024

Language: Английский

Citations

2

SIRT3 alleviates mitochondrial dysfunction and senescence in diabetes-associated periodontitis by deacetylating LRPPRC DOI
Hui Tang, Yiting Zhou, Yu Ye

et al.

Free Radical Biology and Medicine, Journal Year: 2024, Volume and Issue: unknown

Published: Nov. 1, 2024

Language: Английский

Citations

2

Calcium/P53/Ninjurin 1 Signaling Mediates Plasma Membrane Rupture of Acinar Cells in Severe Acute Pancreatitis DOI Open Access

Chehao Lee,

Guang Xin, Fan Li

et al.

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(14), P. 11554 - 11554

Published: July 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

Language: Английский

Citations

6