Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1053/j.gastro.2009.07.037 | DOI Listing |
Nutrients
January 2025
Department of Nutrition, Food Sciences and Physiology, Center for Nutrition and Research, University of Navarra, 31008 Pamplona, Spain.
Background And Aim: Telomere length (TL) is a key biomarker of cellular aging, with shorter telomeres associated with age-related diseases. Lifestyle interventions mitigating telomere shortening are essential for preventing such conditions. This study aimed to examine the effects of two weight loss dietary strategies, based on a moderately high-protein (MHP) diet and a low-fat (LF) diet on TL in individuals with overweight or obesity.
View Article and Find Full Text PDFBiomedicines
January 2025
Department of Anatomy, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo 05508-000, Brazil.
: Aging is associated with structural and functional changes in the heart, including hypertrophy, fibrosis, and impaired contractility. Cellular mechanisms such as senescence, telomere shortening, and DNA damage contribute to these processes. Nuclear factor kappa B (NF-κB) has been implicated in mediating cellular responses in aging tissues, and increased NF-κB expression has been observed in the hearts of aging rodents.
View Article and Find Full Text PDFBiology (Basel)
December 2024
Department of Pediatrics, Medical University of Innsbruck, 6020 Innsbruck, Austria.
Immunosenescence, the age-related decline in immune function, is a complex biological process with profound implications for health and longevity. This phenomenon, characterized by alterations in both innate and adaptive immunity, increases susceptibility to infections, reduces vaccine efficacy, and contributes to the development of age-related diseases. At the cellular level, immunosenescence manifests as decreased production of naive T and B cells, accumulation of memory and senescent cells, thymic involution, and dysregulated cytokine production.
View Article and Find Full Text PDFNature
January 2025
Department of Adult Oncology, Dana Farber Cancer Institute, Boston, Massachusetts, USA.
Telomeres are hypersensitive to the formation of the common oxidative lesion 8-oxoguanine (8oxoG), which impacts telomere stability and function. OGG1 and MUTYH glycosylases initiate base excision repair (BER) to remove 8oxoG or prevent mutation. Here, we show OGG1 loss or inhibition, or MUTYH loss, partially rescues telomeric 8oxoG-induced premature senescence and associated proinflammatory responses, while loss of both glycosylases causes a near complete rescue in human fibroblasts.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!