Abstract: The autophagy-lysosomal pathway (ALP) serves as the primary cellular mechanism for the degradation of dysfunctional proteins and organelles, playing a pivotal role in maintaining intracellular homeostasis and in the cell's response to external stressors. Transcription Factor EB (TFEB), known as a master regulator of autophagy and lysosomal biogenesis, is increasingly recognized in the pathology of various inflammatory conditions. It exerts its influence by activating a suite of genes associated with autophagy, thus not only enhancing the formation and function of lysosomes but also improving the efficiency of autophagosome formation and degradation. This modulation is particularly significant in diseases such as osteoarthritis, atherosclerosis, pancreatitis, inflammatory bowel diseases, and oral inflammatory diseases. In this article, we highlight the critical functions of TFEB and explore its regulatory role in the etiology of inflammatory diseases, offering novel insights and potential therapeutic targets for the development of targeted treatments.

Key words: autophagy-lysosomal pathway, transcription factor EB, inflammatory diseases