Lipofuscin is a representative biomarker of aging that is generated naturally over time. Remofuscin (soraprazan) improves age-related eye diseases by removing lipofuscin from retinal pigment epithelium (RPE) cells. In this study, the effect of remofuscin on longevity in Caenorhabditis elegans and the underlying mechanism were investigated. The results showed that remofuscin significantly (p < 0.05) extended the lifespan of C. elegans (N2) compared with the negative control. Aging biomarkers were improved in remofuscin-treated worms. The expression levels of genes related to lysosomes (lipl-1 and lbp-8), a nuclear hormone receptor (nhr-234), fatty acid beta-oxidation (ech-9), and xenobiotic detoxification (cyp-34A1, cyp-35A1, cyp-35A2, cyp-35A3, cyp-35A4, cyp-35A5, cyp-35C1, gst-28, and gst-5) were increased in remofuscin-treated worms. Moreover, remofuscin failed to extend the lives of C. elegans with loss-of-function mutations (lipl-1, lbp-8, nhr-234, nhr-49, nhr-8, cyp-35A1, cyp-35A2, cyp-35A3, cyp-35A5, and gst-5), suggesting that these genes are associated with lifespan extension in remofuscin-treated C. elegans. In conclusion, remofuscin activates the lysosome-to-nucleus pathway in C. elegans, thereby increasing the expression levels of xenobiotic detoxification genes resulted in extending their lifespan.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9064964 | PMC |
http://dx.doi.org/10.1038/s41598-022-11325-2 | DOI Listing |
Biochem Biophys Res Commun
January 2025
Department of Molecular Medicine, Graduate School of Pharmaceutical Sciences, Kumamoto University, 5-1 Oe-Honmachi, Chuo-ku, Kumamoto, 862-0973, Japan; Global Center for Natural Resources Sciences, Faculty of Life Sciences, Kumamoto University, 5-1 Oe-Honmachi, Chuo-ku, Kumamoto, 862-0973, Japan. Electronic address:
Chem Biol Interact
January 2025
Key Laboratory of Environmental Medicine Engineering, Ministry of Education of China, School of Public Health, Southeast University, Nanjing 210009, Jiangsu, China. Electronic address:
Copper, as a vital trace element and ubiquitous environmental pollutant, exhibits a positive correlation with the neurodegenerative diseases. Recent studies have highlighted ferroptosis's significance in heavy metal-induced neurodegenerative diseases, yet its role in copper-related neurotoxicity remains unclear. This study aimed to investigate the role of ferroptosis in copper-induced neurotoxicity.
View Article and Find Full Text PDFJ Hazard Mater
December 2024
School of Medicine, Yunnan University, Kunming 650091, China. Electronic address:
With the increasing incidence of non-hereditary Parkinson's disease (PD), research into the involvement of specific environmental factors, in addition to aging, has become more prominent. The effects of microplastic exposure on public health have gained increased attention as it is known to cause a range of neurotoxic changes, some of which are similar to the pathological features of PD. We carried out low-dose microplastic exposure experiments on mice and Caenorhabditis elegans models and implemented a survey regarding the utilization of plastic products in the population.
View Article and Find Full Text PDFMar Pollut Bull
January 2025
Department of Bioenvironmental Systems Engineering, National Taiwan University, Taipei 106, Taiwan. Electronic address:
Emerging contaminants in estuarine sediments, such as bis(2-ethylhexyl) phthalate (DEHP) and titanium dioxide nanoparticles (nTiO), pose ecotoxicological risks that may be exacerbated by co-contamination. This study investigated the impacts of DEHP, nTiO, and their combinations at environmentally relevant concentrations (1, 10, and 100 μg/g) on the soil nematode Caenorhabditis elegans in estuarine-like sediment (14.25‰ salinity).
View Article and Find Full Text PDFPLoS One
January 2025
Department of Anesthesiology & Perioperative Medicine, University of Rochester, Rochester, New York, United States of America.
Neurodegenerative diseases are often characterized by mitochondrial dysfunction. In Alzheimer's disease, abnormal tau phosphorylation disrupts mitophagy, a quality control process through which damaged organelles are selectively removed from the mitochondrial network. The precise mechanism through which this occurs remains unclear.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!