Sult2b1, a member of the sulfotransferase family, is responsible for expressing SULT2B1a and SULT2B1b enzymes, which are phase II metabolizing enzymes involved in steroids and hydroxysteroids homeostasis [6]. SULT2B1 is the key enzyme that catalyzes the synthesis of cholesterol sulfate [3]. It is involved in multiple biological pathways, such as lipid metabolism, immune cell regulation, and cell proliferation and migration [1,2,5]. Genetic models, like knockout mice, have been crucial in studying its functions.

In Sult2b1 -/- mice, larger infarction and worse neurological scores were observed after transient middle cerebral artery occlusion, with peripheral monocyte-derived macrophages promoting a pro-inflammatory status [3]. In age-related macular degeneration, Sutl2b1 deficiency reduced leakage areas and inhibited pathological angiogenesis by inhibiting M2 macrophage activation [4]. In colorectal cancer, SULT2B1 knockout suppressed cell proliferation and migration, indicating its oncogenic role [5]. In atherosclerotic mice, knockdown of Sult2b1 led to remission of AS and reduced inflammation levels [7].

In conclusion, Sult2b1 plays essential roles in various biological processes including inflammation, lipid metabolism, and cell proliferation. The use of Sult2b1 knockout mouse models has significantly contributed to understanding its functions in diseases such as ischemic stroke, age-related macular degeneration, colorectal cancer, and atherosclerosis. These findings provide potential therapeutic targets for these diseases.