EXPLORING CELLULAR MECHANISMS IN AGING: INSIGHTS INTO TARGETED INTERVENTIONS FOR AGE-RELATED DISEASES

Abstract

Aging is a complex, multifactorial process driven by cumulative cellular and molecular damage that leads to functional decline and increased susceptibility to chronic diseases. This study investigates the fundamental hallmarks of aging—including genomic instability, mitochondrial dysfunction, epigenetic alterations, and cellular senescence—and evaluates emerging interventions aimed at delaying or reversing age-related deterioration. We identified important senescence triggers like telomere shortening, oxidative stress, and DNA damage that trigger activation of pathways such as p53/p21, NF-  Senescent cells contribute to the disruption of tissue function and promotion of inflammation and they were shown to express different genes (e.g., overexpressed p16, higher IL-6, lower SIRT1, and decreased TERT), and to secrete SASP components (e.g., IL-6 and  It is widespread to see reduced membrane potential and ATP, increased level of ROS and mtDNA damage in aged cells, all of which are highly correlated to age-related disease intensity.  The table and figure analyses revealed that senolytics (Dasatinib + Quercetin), senomorphics (Rapamycin), mitochondrial enhancers (NAD+ precursors) and epigenetic modulators were the most promising treatment classes.  Early clinical studies of these treatments suggest a favorable safety and treatment profile. therefore, these agents are advancing in research now.  Strong relationships between biomarkers such as 8-OHdG and IL-6 with the development of age-related diseases are indicative of their utility for disease monitoring.  Based on a multi-targeted approach targeting the elimination of senescent cells and renewal of mitochondrial function and epigenetic stability, this study claims that aging is modifiable through therapeutic intervention.  Moving forward with these didactic procedures could limit long-term worldwide effects of age-related diseases and even double healthspan.