Aebp1, also known as Adipocyte enhancer-binding protein 1, is a transcriptional repressor. It is involved in regulating critical biological processes such as adipogenesis, mammary gland development, inflammation, macrophage cholesterol homeostasis, and atherogenesis. It participates in multiple signaling pathways, most notably positively regulating the canonical NF-κB pathway by interacting with IκBα, an NF-κB inhibitor [2].

In proliferative diabetic retinopathy, AEBP1 is significantly upregulated in myofibroblast clusters of fibrovascular membranes. siRNA-mediated knockdown of AEBP1 in human retinal pericytes (HRP) reduces the expression of profibrotic markers in high-glucose conditions, suggesting its role in pericyte-myofibroblast transformation and the potential of targeting it to prevent scar tissue formation [1]. In papillary thyroid cancer, knockout of AEBP1 inhibits cell growth, invasion, and EMT marker expression in vitro, and also suppresses tumor growth and lung metastasis in xenograft models, with BMP4 identified as a downstream target [3]. In cisplatin-resistant oral cancer cells, silencing of AEBP1 inhibits cell proliferation, migration, and invasion, and predisposes cells to ferroptosis via the JNK/p38/ERK pathway [4].

In conclusion, Aebp1 plays crucial roles in multiple biological processes and disease conditions. Through gene-knockout or knockdown models in various cell lines and animal models, its functions in fibrosis-related diseases like diabetic retinopathy, and in cancer progression in different cancer types, have been revealed. These findings suggest that Aebp1 could be a potential therapeutic target for these diseases.