<p>Replicative senescence frequently occurs in in vitro cell cultures and certain in vivo pathological conditions, characterized by multiple phenotypes, including cell cycle arrest. Previous studies suggested that the main mechanism underlying replicative senescence is that under continuous subculture, cells sense DNA damage during G1, which triggers G1/S arrest and the subsequent geroconversion. However, this explanation does not account for phenomena such as how DNA damage caused by replication stress in the mother cell directly affects the G1/S transition in the daughter cell. Recent advances in single-cell analysis techniques have enabled more detailed investigation of the G1/S transition process, leading to the development of new models. The updated model extends the window for cells to sense DNA damage from daughter G1 backward to mother G2, significantly prolonging the period during which DNA damage can regulate the G1/S transition. Despite these developments, the mechanistic understanding of replicative senescence has not been comprehensively revised based on the updated model. Therefore, this review systematically elaborates on the key process of G1/S arrest in inducing replicative senescence, based on the existing evidence: DNA damage accumulated during continuous passaging activates the p53-p21 and p16-Rb pathways at different cell cycle stages. The p53-p21 pathway promotes the initiation and progression of replicative senescence by primarily inactivating cyclin-dependent kinase complexes during mother G2 and daughter G1, thereby temporarily arresting the cell cycle. In the final stages of replicative senescence, the p16-Rb pathway predominantly substitutes for p21 to enforce an irreversible cell cycle arrest. The geroconversion process associated with these pathways ultimately facilitates the emergence of diverse senescence phenotypes.</p>