Document Type : Review Article
Authors
1
medical physiology department at sohag faculty of medicine
2
Department of histology, Faculty of medicine, Sohag university.
3
Medical Physiology department, Sohag Faculty of Medicine, Sohag university
4
physiology department.faculty of medicine,sohag university.
5
Department of Dermatology, Faculty of medicine, Sohag University, Sohag, Egypt
6
Department of Physiology, Faculty of Medicine, Sohag University, Sohag, Egypt.
10.21608/smj.2025.408634.1596
Abstract
Aging is a complex, time-dependent decline in human function, increasingly affecting the global population, particularly those over 65. With advancements in medical technology, lifespan has increased, but so has the prevalence of age-related disorders such as cardiovascular diseases, cancer, and neurodegenerative diseases. This decline is driven by cellular senescence, oxidative stress, and inflammation. Multiple theories of aging have been proposed, encompassing both programmed and damage-induced perspectives.
Many studies examine the biochemical and genetic mechanisms underlying the aging process, which encompasses telomere shortening, genomic instability, oxidative stress, cellular senescence, and epigenetic changes. Aging significantly contributes to various age-related disorders, including neurodegenerative diseases, cardiovascular diseases. Key findings include the role of genomic instability due to DNA damage accumulation, the impact of reduced telomere length on cellular senescence, mitochondrial dysfunction related to energy production and ROS generation, and the decline in proteostasis leading to protein aggregation. Understanding these pathways may provide targets for interventions aimed at delaying aging and ameliorating related diseases.
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