Basp1, also known as Brain Acid Soluble Protein 1, is a membrane-bound protein that plays diverse roles in various biological processes. It is involved in regulating actin dynamics and presynaptic vesicle cycling at axon terminals, thus facilitating axonal growth, regeneration, and plasticity [3]. It also functions as a transcriptional corepressor, modifying chromatin through lipid-dependent and lipid-independent mechanisms [5].

In diet-induced NASH (non-alcoholic steatohepatitis) in mice, myeloid-specific inactivation of Basp1 attenuates the severity of NASH pathologies, including reduced hepatocyte injury and liver fibrosis. Mechanistically, macrophages lacking Basp1 exhibit a diminished response to pro-inflammatory stimuli, impaired NLRP3 inflammasome activation, and reduced cytokine secretion [1].

In osteoclastogenesis, knocking down BASP1 expression in bone marrow macrophages enhanced RANKL-induced osteoclastogenesis, promoted cell-cell fusion, and increased mineral degrading abilities [2].

In gliomas, downregulation of BASP1 promotes temozolomide resistance through epigenetic activation of the FBXO32/NF-κB/MGMT axis [4].

In osteoarthritis, BASP1 knockdown alleviates chondrocyte apoptosis and extracellular matrix degradation in vivo and in vitro [6].

In conclusion, Basp1 is a multi-functional gene involved in processes such as axonal regulation, chromatin modification, and inflammation-related disease progression. Gene knockout and conditional knockout mouse models have been crucial in revealing its role in diseases like NASH, osteoclast-related bone diseases, gliomas, and osteoarthritis, providing potential therapeutic targets for these conditions.