Sperm freezing damage is a critical issue in cryopreservation, with cellular death playing a central role. This review explores the mechanisms of sperm freezing damage, focusing on regulated cell death (RCD) and accidental cell death (ACD). RCD includes apoptosis, ferroptosis, necroptosis, and cuproptosis, while ACD involves physical damage from intracellular ice crystals. Oxidative stress is a major contributor to sperm freezing damage, inducing various RCD pathways. The cooling rate during freezing is crucial, as it balances dehydration and ice crystal formation, known as the "two-factor hypothesis." Glycerol, a permeable cryoprotectant, reduces intracellular ice crystal formation but does not fully prevent sperm death. Despite advances in cryopreservation, approximately 40–50% of sperm still die after freezing, with surviving sperm showing functional impairments. Oxidative stress, caused by reactive oxygen species (ROS), leads to lipid peroxidation and mitochondrial damage, triggering RCD. Apoptosis is the only RCD marker identified in sperm freezing damage, but other RCD types like ferroptosis and necroptosis may also be involved. Ferroptosis, linked to lipid peroxidation and iron regulation, is a key pathway in sperm freezing damage. Necroptosis, a form of regulated necrosis, can be triggered by oxidative stress and is associated with increased ROS levels. Cuproptosis, involving copper accumulation, may also contribute to sperm damage. Autophagy, a cellular stress response, can either protect or promote cell death, depending on its regulation. The interplay between different RCD types, including calcium signaling and autophagy, is complex and requires further investigation. Understanding these mechanisms is essential for improving sperm cryopreservation techniques and enhancing the quality of thawed semen.Sperm freezing damage is a critical issue in cryopreservation, with cellular death playing a central role. This review explores the mechanisms of sperm freezing damage, focusing on regulated cell death (RCD) and accidental cell death (ACD). RCD includes apoptosis, ferroptosis, necroptosis, and cuproptosis, while ACD involves physical damage from intracellular ice crystals. Oxidative stress is a major contributor to sperm freezing damage, inducing various RCD pathways. The cooling rate during freezing is crucial, as it balances dehydration and ice crystal formation, known as the "two-factor hypothesis." Glycerol, a permeable cryoprotectant, reduces intracellular ice crystal formation but does not fully prevent sperm death. Despite advances in cryopreservation, approximately 40–50% of sperm still die after freezing, with surviving sperm showing functional impairments. Oxidative stress, caused by reactive oxygen species (ROS), leads to lipid peroxidation and mitochondrial damage, triggering RCD. Apoptosis is the only RCD marker identified in sperm freezing damage, but other RCD types like ferroptosis and necroptosis may also be involved. Ferroptosis, linked to lipid peroxidation and iron regulation, is a key pathway in sperm freezing damage. Necroptosis, a form of regulated necrosis, can be triggered by oxidative stress and is associated with increased ROS levels. Cuproptosis, involving copper accumulation, may also contribute to sperm damage. Autophagy, a cellular stress response, can either protect or promote cell death, depending on its regulation. The interplay between different RCD types, including calcium signaling and autophagy, is complex and requires further investigation. Understanding these mechanisms is essential for improving sperm cryopreservation techniques and enhancing the quality of thawed semen.