98%
921
2 minutes
20
Intestinal aging is central to systemic aging, characterized by a progressive decline in intestinal structure and function. The core mechanisms involve dysregulation of epithelial cell renewal and gut microbiota dysbiosis. In addition to previous results in model organisms like , recent studies have shown that in mammalian models, aging causes increased intestinal permeability and intestinal-derived systemic inflammation, thereby affecting longevity. Therefore, anti-intestinal aging can be an important strategy for reducing frailty and promoting longevity. There are three key gaps remaining in the study of intestinal aging: (1) overemphasis on aging-related diseases rather than the primary aging mechanisms; (2) lack of specific drugs or treatments to prevent or treat intestinal aging; (3) limited aging-specific dysbiosis research. In this review, the basic structures and renewal mechanisms of intestinal epithelium, and mechanisms and potential therapies for intestinal aging are discussed to advance understanding of the causes, consequences, and treatments of age-related intestinal dysfunction.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12278430 | PMC |
http://dx.doi.org/10.1016/j.apsb.2025.05.011 | DOI Listing |
Environ Geochem Health
September 2025
Policy Research Center for Environment and Economy, Ministry of Ecology and Environment of the People's Republic of China, Beijing, 100101, China.
The behavior of polycyclic aromatic hydrocarbons (PAHs) released from tire road wear particles (TRWPs) in human digestive fluids may pose a significant risk to human health. However, the current understanding of the release pattern and influencing factors of PAHs from TRWPs is still insufficient. In this study, the release characteristics of PAHs from UV-aging TRWPs (ATRWPs) were systematically investigated by in vitro digestive simulation experiments, release kinetic model fitting and control variable experiments.
View Article and Find Full Text PDFAutophagy Rep
September 2025
Department of Cell Biology, School of Medicine of Ribeirão Preto, University of São Paulo, São Paulo, Brazil.
Autophagy is an evolutionarily conserved cellular process that is prominent during bacterial infections. In this review article, we discuss how direct pathogen clearance via xenophagy and regulation of inflammatory products represent dual functions of autophagy that coordinate an effective antimicrobial response. We detail the molecular mechanisms of xenophagy, including signals that indicate the presence of an intracellular pathogen and autophagy receptor-mediated cargo targeting, while highlighting pathogen counterstrategies, such as bacterial effector proteins that inhibit autophagy initiation or exploit autophagic membranes for replication.
View Article and Find Full Text PDFActa Biochim Biophys Sin (Shanghai)
September 2025
Zhejiang University School of Medicine, Hangzhou 310058, China.
Intestinal immunosenescence, a hallmark of organismal aging, has emerged as a critical biological process impacting the health of elderly individuals. This review systematically examines the core mechanisms underlying intestinal immunosenescence, including immune cell dysfunction, imbalances in immune-microbiota interactions, and impaired barrier function. We analyze its associations with infectious diseases, chronic inflammation, and neurodegenerative disorders, summarizing recent advances in dietary interventions, microecological therapy, and other emerging strategies.
View Article and Find Full Text PDFInt J Biol Macromol
September 2025
Cancer Biology Program, University of Hawaii Cancer Center, University of Hawaii at Manoa, 701 Ilalo Street, Hawaii, HI 96813, USA. Electronic address:
RGPR-p117 is a newly discovered transcription factor that specifically binds to the nuclear factor I consensus motif, TTGGC(N)CC, in the promoter region of the regucalcin gene. This gene plays a multifunctional role in cell regulation. The human RGPR-p117 gene comprises 26 exons totaling approximately 4.
View Article and Find Full Text PDF