Preterm labor is a major contributor to neonatal mortality and morbidity worldwide. Despite extensive research, the molecular mechanisms driving preterm labor are not fully understood. Epigenetic modifications may play a role in the underlying mechanisms leading to adverse pregnancy outcomes, particularly preterm labor. Emerging evidence highlights the role of microRNAs (miRNAs), small non-coding RNAs that regulate gene expression post-transcriptionally, in the pathogenesis of preterm labor. This review focuses on the chorioamniotic membrane, a critical structure for fetal protection and development, and its involvement in miRNA-mediated pathways that contribute to preterm labor. The chorioamniotic membrane, composed of the amnion and chorion, plays a vital role in maintaining pregnancy through extracellular matrix (ECM) remodeling, immune regulation, and inflammatory responses. Dysregulation of miRNAs in this membrane, influenced by environmental stressors (e.g., oxidative stress, pollutants), maternal factors (e.g., age, obesity, diabetes), and fetal factors (e.g., sex, genetic disorders), disrupts these processes, leading to membrane weakening and preterm labor. Inflammation, particularly through Toll-like receptor (TLR) signaling and cytokine production, is a key driver of miRNA dysregulation in conditions like chorioamnionitis and preterm premature rupture of membranes (PPROM). This review summarizes the dysregulated expression of miRNAs in chorioamniotic membranes which are likely to play a role in premature birth.