The epithelial-mesenchymal transition (EMT) is a critical process in embryonic development, tissue repair, and disease progression, including organ fibrosis and cancer. EMT involves the induction of transcription factors that alter gene expression, leading to the loss of cell-cell adhesion and a shift in cytoskeletal dynamics. Key transcription factors involved in EMT include Snail1/2, ZEB1/2, Twist, and LEF-1, which repress the expression of E-cadherin and other epithelial markers. The activation of EMT is mediated by various signaling pathways, including TGF-β, BMP, Wnt-β-catenin, Notch, Hedgehog, and receptor tyrosine kinases. These pathways are activated by local microenvironmental cues such as growth factors, cytokines, hypoxia, and extracellular matrix (ECM) interactions. The crosstalk between these pathways and their response to microenvironmental signals regulate the expression and function of EMT-inducing transcription factors. Understanding these mechanisms is crucial for therapeutic control of EMT to promote tissue regeneration, treat fibrosis, and prevent cancer metastasis.The epithelial-mesenchymal transition (EMT) is a critical process in embryonic development, tissue repair, and disease progression, including organ fibrosis and cancer. EMT involves the induction of transcription factors that alter gene expression, leading to the loss of cell-cell adhesion and a shift in cytoskeletal dynamics. Key transcription factors involved in EMT include Snail1/2, ZEB1/2, Twist, and LEF-1, which repress the expression of E-cadherin and other epithelial markers. The activation of EMT is mediated by various signaling pathways, including TGF-β, BMP, Wnt-β-catenin, Notch, Hedgehog, and receptor tyrosine kinases. These pathways are activated by local microenvironmental cues such as growth factors, cytokines, hypoxia, and extracellular matrix (ECM) interactions. The crosstalk between these pathways and their response to microenvironmental signals regulate the expression and function of EMT-inducing transcription factors. Understanding these mechanisms is crucial for therapeutic control of EMT to promote tissue regeneration, treat fibrosis, and prevent cancer metastasis.