Lpcat4, also known as LPLAT10 and LPEAT2, is a lysophosphatidylcholine acyltransferase that plays a key role in phospholipid remodeling. It is involved in the Lands' cycle, which is crucial for the maturation and maintenance of the fatty acid composition of biomembranes. Phospholipid remodeling is associated with multiple biological processes including cell differentiation, metabolism, and maintaining barrier integrity [1,2,4]. Genetic models, such as gene knockout (KO) and conditional knockout (CKO) mouse models, can be valuable for studying Lpcat4 function.

In urothelial cells, Lpcat4 knockdown led to impaired proliferation, altered trans-epithelial electrical resistances, and reduced capacity to restore barrier function after wounding, suggesting its importance in urothelial barrier integrity [1]. In hepatocellular carcinoma, Lpcat4 enhanced cell growth and cholesterol biosynthesis by up-regulating ACSL3 through the WNT/β-catenin/c-JUN signaling pathway, indicating its role in cancer development [3]. In ATDC5 cells, Lpcat4 knockdown decreased chondrogenic markers, suggesting its importance in chondrogenic differentiation [4].

In conclusion, Lpcat4 is essential for processes like cell-specific barrier integrity, chondrogenic differentiation, and is involved in cancer-related pathways. Studies using KO/CKO mouse models have provided insights into its role in urothelial function, chondrogenesis, and hepatocellular carcinoma, highlighting its potential as a therapeutic target in certain disease areas.