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The process of aging is a complicated biological phenomenon that is marked by a loss of functionalities and high susceptibility to illness. Recent developments in geroscience have narrowed down the classical paradigm of aging processes into the so-called Hallmarks of Aging 2.0 where molecular pathways including genomic instability, epigenetic changes, mitochondrial dysfunction, chronic inflammation, and cellular senescence are connected. The buildup of senescent cells also known as the zombie cells has come out as one of the major causes of tissue degeneration during the aging process. These cells are metabolically active and irreversibly differentiate but continue to secrete pro-inflammatory factors referred to as senescence-associated secretory phenotype (SASP). There are two key therapeutic approaches that have been optimized to combat cellular senescence; senolytics, which are specific to eliminate senescent cells, and senomorphics, which inhibit the pathogenic secretory phenotype of senescent cells, but do not kill them. The current review presents an overview of the current results of animal-based experimental research on the molecular hallmark of aging and compares the relative efficacy of senolytic and senomorphic treatment in regulating aging pathways. The article identifies the most important experimental models, mechanisms of action, therapeutic potential and limitations of the existing approaches. The knowledge of these strategies offers an insightful critical view of longevity science and can lead to new possibilities in creating anti-aging interventions to work on basic biological processes.