Lama4, encoding laminin α4, is a major receptor-binding chain of several laminins and an important component of the extracellular matrix in various tissues [1,2]. Laminins play crucial roles in cell adhesion, migration, proliferation, and differentiation, and Lama4 is involved in maintaining the integrity and function of the extracellular matrix and cell-matrix interactions.

In gene-knockout studies, Lama4 deletion in mice led to impaired hematopoiesis regeneration after irradiation-induced stress, accompanied by altered bone marrow niche composition and inflammation. In a transplantation-induced MLL-AF9 AML mouse model, Lama4 -/- mice showed accelerated AML progression and relapse. Lama4 -/- mesenchymal stem cells had molecular alterations, promoting AML stem cell proliferation and chemoresistance [1]. In preeclampsia research, down-regulation of the LAMA4 gene in HTR-8/SVneo cells (modeling extravillous trophoblasts) inhibited cell proliferation, migration, and invasion, and affected the expression of vascular factors [3].

In conclusion, Lama4 is essential for normal hematopoiesis regeneration and maintaining the balance of the bone marrow niche. Its absence promotes acute myeloid leukemia progression. In preeclampsia, the regulation of LAMA4 expression may be a potential therapeutic target. The use of Lama4 knockout mouse models has significantly contributed to understanding its role in these disease-related biological processes.