Aging is characterized by progressive deterioration of physiological integrity, decline in homeostasis, and degeneration of the tissues that occurs after the reproductive phase of life is complete, leading to impaired function. This deterioration is an important risk factor for chronic lung pathologies such as chronic obstructive pulmonary disease (COPD). COPD is a disease that develops gradually. Emphysematous changes in the lung take years to develop after exposure to cigarette smoke; hence, the vast majority of patients are elderly. There has been a dramatic increase in the life expectancy of the general population, resulting in an increased burden of chronic lung diseases. There is growing evidence that molecular mechanisms involved in aging may also play a role in COPD pathogenesis. Recently, the nine hallmarks of aging were identified. In this article, we will review the nine hallmarks of aging and how each hallmark contributes to the pathogenesis of COPD.
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http://dx.doi.org/10.4103/lungindia.lungindia_266_17 | DOI Listing |
Aging (Albany NY)
January 2025
Department of Pathology, Yale University School of Medicine, New Haven, CT 06519, USA.
Studies of the aging transcriptome focus on genes that change with age. But what can we learn from age-invariant genes-those that remain unchanged throughout the aging process? These genes also have a practical application: they can serve as reference genes in expression studies. Reference genes have mostly been identified and validated in young organisms, and no systematic investigation has been done across the lifespan.
View Article and Find Full Text PDFLife Med
June 2024
Laboratory of Stem cell and anti-Aging Research, Frontiers Science Center for Disease-related Molecular Network, State Key Laboratory of Respiratory Health and Multimorbidity and National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu 610041, China.
The decline in intestinal stem cell (ISC) function is a hallmark of aging, contributing to compromised intestinal regeneration and increased incidence of age-associated diseases. Novel therapeutic agents that can rejuvenate aged ISCs are of paramount importance for extending healthspan. Here, we report on the discovery of Chrysosplenosides I and A (CAs 1 & 2), flavonol glycosides from the Xizang medicinal plant Maxim.
View Article and Find Full Text PDFDietary protein is a key regulator of healthy aging in both mice and humans. In mice, reducing dietary levels of the branched-chain amino acids (BCAAs) recapitulates many of the benefits of a low protein diet; BCAA-restricted diets extend lifespan, reduce frailty, and improve metabolic health, while BCAA supplementation shortens lifespan, promotes obesity, and impairs glycemic control. Recently, high protein diets have been shown to promote cellular senescence, a hallmark of aging implicated in many age-related diseases, in the liver of mice.
View Article and Find Full Text PDFHematopoietic aging is characterized by chronic inflammation associated with myeloid bias, HSC accumulation, and functional HSC impairment. Yet it remains unclear how inflammation promotes these aging phenotypes. NFkappaB both responds to and directs inflammation, and we present an experimental model of elevated NFkappaB activity (IkappaBminus) to dissect its role in hematopoietic aging phenotypes.
View Article and Find Full Text PDFBackground: A significant proportion of individuals maintain healthy cognitive function despite having extensive Alzheimer's disease (AD) pathology, known as cognitive resilience. Understanding the molecular mechanisms that protect these individuals can identify therapeutic targets for AD dementia. This study aims to define molecular and cellular signatures of cognitive resilience, protection and resistance, by integrating genetics, bulk RNA, and single-nucleus RNA sequencing data across multiple brain regions from AD, resilient, and control individuals.
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