Autophagy and apoptosis are catabolic pathways essential for homeostasis. They play a crucial role for normal placental and fetal development. These cell death mechanisms are exaggerated in placental disorders such as preeclampsia, intrauterine growth restriction (IUGR) and gestational diabetes mellitus (GDM). Apoptosis is widely studied, highly controlled and regulated whereas; autophagy is an orderly degradation and recycling of the cellular components. Cellular senescence may be initiated by a variety of stimuli, including hypoxia, oxidative stress, reduction in survival signals and nutrition deprivation. Apoptosis is regulated by two types of pathways intrinsic and extrinsic. Extrinsic pathway is initiated by apoptosis inducing cells such as macrophages, natural killer cells whereas; intrinsic pathway is initiated in response to DNA damage, cell injury and lack of oxygen. In autophagy, the cell or organelles undergo lysosomal degradation. Placental apoptosis increases as the gestation progresses while autophagy plays a role in trophoblast differentiation and invasion. In pregnancy disorders like preeclampsia and IUGR, proapoptotic markers such as caspase 3, 8, BAX are higher and antiapoptotic markers like Bcl-2 are lower. In GDM, apoptotic markers are reduced resulting in increased placental mass and fetal macrosomia. Apoptosis in the pathological pregnancies is also influenced by the reduced levels of micronutrients and long chain polyunsaturated fatty acids resulting in disturbed placental biology. This chapter describes the role of various key molecular events involved in cellular senescence and the various factors influencing them. This will help identify future therapeutic strategies for better management of these processes.