Pathophysiology of human aging with a hint on sarcopenia: A review article. | ||
Sohag Medical Journal | ||
Volume 29, Issue 3, 2025, Pages 231-238 PDF (1.22 M) | ||
Document Type: Review Article | ||
DOI: 10.21608/smj.2025.408634.1596 | ||
Authors | ||
Alshymaa Mohamed Farouk* 1; Nesreen Abd El-Haliem2; dina monir hegab3; Seham Abd-Alrahman Abd-allatif4; Sara Hassan5; Amany Abdelrahman Abdelhamid6 | ||
1medical physiology department at sohag faculty of medicine | ||
2Department of histology, Faculty of medicine, Sohag university. | ||
3Medical Physiology department, Sohag Faculty of Medicine, Sohag university | ||
4physiology department.faculty of medicine,sohag university. | ||
5Department of Dermatology, Faculty of medicine, Sohag University, Sohag, Egypt | ||
6Department of Physiology, Faculty of Medicine, Sohag University, Sohag, Egypt. | ||
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. | ||
Keywords | ||
Pathophysiology; human aging; sarcopenia | ||
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