The endoplasmic reticulum (ER) protein stearoyl-CoA desaturase (SCD), which has a high turnover rate and functions as a model for the selective degradation of short-lived proteins, is a key regulator of membrane fluidity. A key player in the catalysis of the synthesis of monounsaturated fatty acids, primarily oleate and palmitoleate, is the rate-limiting lipogenic enzyme known as SCD. Each makes a significant contribution to the biological membrane. Several SCD isoforms, including SCD-1 and SCD-5 in humans and SCD-1 and SCD-4 in mice, are present.
Diabetes and non-alcoholic fatty liver disease are two metabolic diseases that exhibit overexpression of SCD. SCD promotes tumorigenesis and stemness by activating the YAP pathway and the canonical Wnt pathway. SCD promotes metabolic reprogramming in cancer, which is at least partially mediated by MUFA-mediated control of AKT, AMPK, and NF-kB. From a biological perspective, excessive SCD1 expression results in a variety of metabolic diseases, such as obesity, insulin resistance, hypertension, hypertriglyceridemia, etc. SCD1 is a pharmacological target in the treatment of metabolic diseases like diabetes, obesity, and others.
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