Cellular senescence, identified as a state of permanent cell cycle arrest, has become central to understanding aging and disease. Initially seen as a cellular aging mechanism, it is now recognized for its roles in development, tissu repair and tumour suppression. However, the accumulation of senescent cells with age contributes to chronic diseases such as diabetes, atherosclerosis and neurodegeneration. Recent efforts have focused on “senotherapeutics”, including senolytics, which aim to eliminate senescent cells to mitigate age-related decline. Despite significant advances, senescence research faces critical challenges because of inconsistent detection methods. Common markers, such as p16INK4a and senescence-associated β-galactosidase, vary across tissues and contexts, complicating cross-study comparisons and clinical applications. A standardized multifaceted approach to senescence detection is essential, and should incorporate complementary methods, clear thresholds for senescence classification and considerations for cell type-specific variations. Such standardization would enhance reproducibility, streamline research and facilitate clinical translation, advancing therapeutic applications in aging and disease management.