Stab1, encoding the multifunctional scavenger receptor stabilin-1, is preferentially expressed by liver sinusoidal endothelial cells. It mediates the clearance of circulating plasma molecules, thus controlling distant organ homeostasis [1]. It has also been associated with the regulation of the IKK/NF-κB pathway [2].

In ApoE-KO mice interbred with Stab1-KO mice, spontaneous and Western diet-associated atherogenesis was significantly reduced, suggesting that targeting Stab1 can ameliorate atherosclerosis [1]. In acute myeloid leukemia (AML), STAB1 knockdown in human AML cell lines HEL and NB4 suppressed proliferation and promoted apoptosis through regulating the IKK/NF-κB pathway, and STAB1 silencing prolonged survival in xenograft mouse models [2]. In malignant mesothelioma, STAB1 was among the genes that could potentially be specific therapeutic targets as monocyte-derived macrophages expressing STAB1 play a role in tumor development [3]. In cytogenetically normal AML (CN-AML), high STAB1 expression was associated with poor outcomes, and STAB1 suppression inhibited cell growth in KG1a and NB4 leukemia cells [4].

In conclusion, Stab1 is crucial for plasma molecule clearance and organ homeostasis. Gene-knockout mouse models have revealed its role in diseases such as atherosclerosis, AML, and malignant mesothelioma. Targeting Stab1 may offer potential therapeutic strategies for these diseases.