Autophagy is a cellular bulk destructive mechanism in which a part of the cytoplasm is encapsulated in double membrane-bound structures termed autophagosomes, which can be matured and fused with lysosomes for dilapidation (Klionsky and Emr, 2000, Levine and Klionsky, 2004). Originally, autophagy is assumed to be a survival mechanism in response to insufficient food and other types of cellular stresses (Yorimitsu and Klionsky 2005). According to the findings of several types of research, autophagy seems to stimulate cell death by excessive self-degradation and destruction of the critical cellular elements (Gozuacik and Kimchi, 2004, Eskelinen, 2005). Additionally, earlier research has indicated that autophagy may be induced by a variety of triggers and circumstances causing apoptosis (Kessel et al., 2006, Kunchithapautham and Rohrer, 2007). According to a growing body of research, basal autophagy is required to sustain the endometrial homeostasis and endometrial-specific processes modulation, such as menstruation, implantation, and decidualization (Kunchithapautham and Rohrer, 2007, Popli et al., 2021). A successful pregnancy relies heavily on proper decidualization. Many pregnancy disorders that clinically appear in the first trimester, such as miscarriage, preterm birth (PTB), fetal growth restriction (FGR), and preeclampsia (PE), are originated from implantation or placentation disorder in early gestation (Cross et al., 1994, Norwitz et al., 2001, Cha et al., 2012). Despite extensive study and a substantially enhanced knowledge of the cellular and molecular mechanisms behind implantation and placentation, strategies to prevent these issues have generally failed. Humans’ decidualization occurs during the second half of each menstrual cycle, thus is unaffected by the conceptus and regulated by many factors (Emera et al., 2012, Jarrell, 2018). This review highlights the genes, pathways, regulation, and function of autophagy in endometrial decidualization, as well as other factors involved in the process.