Male sex determination maintains proteostasis and extends lifespan of daf-18/PTEN deficient C. elegans.

Although females typically have a survival advantage, those with PTEN functional abnormalities face a higher risk of developing tumors than males. However, the differences in how each sex responds to PTEN dysfunction have rarely been studied. We use Caenorhabditis elegans to investigate how male and hermaphrodite worms respond to dysfunction of the PTEN homolog daf-18.

Cysteine protease cathepsin B promotes lysosome integrity to extend the lifespan of alternative day fasting worms.

Alternative day fasting (ADF) has been shown to enhance the lifespan of animals. However, human trials evaluating the efficacy of ADF have only recently emerged, presenting challenges due to the extreme nature of this dietary regimen. To better understand the effects of ADF, we investigated its impact using Caenorhabditis elegans as a model organism.

Inhibiting HSD17B8 suppresses the cell proliferation caused by PTEN failure.

Loss of the tumor suppressor PTEN homolog daf-18 in Caenorhabditis elegans (C. elegans) triggers diapause cell division during L1 arrest. While prior studies have delved into established pathways, our investigation takes an innovative route.

Cadmium-induced reproductive toxicity combined with a correlation to the oogenesis process and competing endogenous RNA networks based on a Caenorhabditis elegans model.

Accumulation of the heavy metal Cadmium (Cd) in the ovaries and placenta can affect the structure and function of these organs and induce female reproductive toxicity. This toxicity may be due to Cd's similarity to estrogen and its ability to disrupt endocrine systems. However, the exact molecular mechanism by which Cd causes reproductive toxicity at the transcriptome level remains poorly understood.

Effect of self-management intervention on prognosis of patients with chronic heart failure: A meta-analysis.

Aim: The purpose of this study is to explore the influence of self-management intervention on four prognostic indicators of readmission rate, mortality rate, self-management ability and quality of life in patients with chronic heart failure.

Design: A meta-analysis.

Methods: This study was selected from the related studies published from January 1999 to January 2022, and was searched by searching five databases: PubMed, Science of Website, China National Knowledge Infrastructure (CNKI), Wan Fang and Wei Pu (VIP).

Vitamin K2 Enhances Fat Degradation to Improve the Survival of .

The beneficial effects of vitamin K (VK) on various chronic age-related syndromes have generally been considered dependent on its antioxidant effects. However, due to the distinct bioavailability and biological activities of VKs, exactly which of these activities and by what mechanisms they might act still need to be elucidated. In this study, we found that VK2 can extend the lifespan of and improve the resistance to pathogen infection, heat stress and HO-induced inner oxidative stress.

The Review of Anti-aging Mechanism of Polyphenols on .

Micronutrients extracted from natural plants or made by biological synthesis are widely used in anti-aging research and applications. Among more than 30 effective anti-aging substances, employing polyphenol organic compounds for modification or delaying of the aging process attracts great interest because of their distinct contribution in the prevention of degenerative diseases, such as cardiovascular disease and cancer. There is a profound potential for polyphenol extracts in the research of aging and the related diseases of the elderly.

BRAF Controls the Effects of Metformin on Neuroblast Cell Divisions in .

Metformin has demonstrated substantial potential for use in cancer treatments. Liver kinase B (LKB)-AMP-activated protein kinase (AMPK) and mTOR are reported to be the main targets of metformin in relation to its ability to prevent cancer cell proliferation. However, the role of metformin in the control of neoplastic cancer cell growth is possibly independent of LKB-AMPK and mTOR.

Glucose and cholesterol induce abnormal cell divisions via DAF-12 and MPK-1 in .

People exposed to starvation have a high risk of developing cancer later in life, and prior studies have shown these individuals have high insulin and cholesterol levels and are sensitive to glucose. Using as a model, we found that glucose and cholesterol can promote survival and cause starved L1 diapause worms to undergo abnormal neuronal cell divisions. Starvation has also been shown to promote long-term survival; however, we found that the functions of glucose and cholesterol in relation to these cell divisions are distinct from their effects on survival.

PTEN and AMPK block neuroblast divisions by inhibiting a BMP-insulin-PP2A-MAPK pathway.

that hatch in the absence of food stop their postembryonic development in a process called L1 arrest. Intriguingly, we find that the postembryonic Q neuroblasts divide and migrate during L1 arrest in mutants that have lost the energy sensor AMP-activated protein kinase (AMPK) or the insulin/IGF-1 signaling (IIS) negative regulator DAF-18/PTEN. We report that DBL-1/BMP works upstream of IIS to promote agonistic insulin-like peptides during L1 arrest.

A functional study of all 40 insulin-like peptides.

The human genome encodes 10 insulin-like genes, whereas the genome remarkably encodes 40 insulin-like genes. Knockout strategies to determine the roles of all the insulin/insulin-like peptide ligands (INS) in has been challenging due to functional redundancy. Here, we individually overexpressed each of the 40 genes pan-neuronally, and monitored multiple phenotypes including: L1 arrest life span, neuroblast divisions under L1 arrest, dauer formation, and fat accumulation, as readouts to characterize the functions of each INS Of the 40 INS peptides, we found functions for 35 INS peptides and functionally categorized each as agonists, antagonists, or of pleiotropic function.

Chlorogenic Acid Extends the Lifespan of Caenorhabditis elegans via Insulin/IGF-1 Signaling Pathway.

Coffee and tea, two of the most popular drinks around the world, share many in common from chemical components to beneficial effects on human health. One of their shared components, the polyphenols, most notably chlorogenic acid (CGA), was supposed to account for many of the beneficial effects on ameliorating diseases occurred accompanying people aging, such as the antioxidant effect and against diabetes and cardiovascular disease. CGA is also present in many traditional Chinese medicines.

C. elegans Methods to Study PTEN.

C. elegans encodes a PTEN homolog called DAF-18 and human PTEN can functionally replace DAF-18. Thus C.

Mulberry leaf polyphenols delay aging and regulate fat metabolism via the germline signaling pathway in Caenorhabditis elegans.

Mulberry leaves are an important ingredient in some traditional Chinese medicinal formulas and has been developed for use in functional food products. The antioxidant activity of mulberry leaf extract has been reported to have beneficial effects on diseases in vitro; however, it is not clear which components in mulberry leaf extracts have these functions. Furthermore, the mechanisms of action of these ingredients have not been extensively investigated.

Mulberry leaf phenolics ameliorate hyperglycemia-induced oxidative stress and stabilize mitochondrial membrane potential in HepG2 cells.

To investigate the effect of phenolics in mulberry leaves (mulberry leaf phenolics; MLP) on hyperglycemia-induced oxidative stress and mitochondrial membrane potential (ΔΨm) in HepG2 cells; we treated HepG2 with glucose [5.5 (N-Glc) or 50 mmol/L (Hi-Glc)] with or without MLP at 10 or 100 µmol/L gallic acid equivalents and assessed level of reactive oxidant species (ROS), ΔΨm, malondialdehyde (MDA) and nuclear factor-kappaB (NF-κB) activation. Hi-Glc-induced oxidative damage was demonstrated by a series of increase in superoxides (560%, 0.

ins-7 Gene expression is partially regulated by the DAF-16/IIS signaling pathway in Caenorhabditis elegans under celecoxib intervention.

DAF-16 target genes are employed as reporters of the insulin/IGF-1 like signal pathway (IIS), and this is notably true when Caenorhabditis elegans (C. elegans) is used to study the action of anti-aging compounds on IIS activity. However, some of these genes may not be specific to DAF-16, even if their expression levels are altered when DAF-16 is activated.

Aspirin extends the lifespan of Caenorhabditis elegans via AMPK and DAF-16/FOXO in dietary restriction pathway.

Aspirin has been revealed to have many beneficial effects for health since it was discovered as a nonsteroidal anti-inflammatory drug (NSAID) to treat pain and inflammation. Here, we investigated the molecular mechanism of aspirin on the lifespan extension of Caenorhabditis elegans. Our results showed that aspirin could extend the lifespan of C.

Drug absorption efficiency in Caenorhbditis elegans delivered by different methods.

Background: Caenorhbditis elegans has being vigorously used as a model organism in many research fields and often accompanied by administrating with various drugs. The methods of delivering drugs to worms are varied from one study to another, which make difficult in comparing results between studies.

Methodology/principal Findings: We evaluated the drug absorption efficiency in C.