LAMB1, or laminin subunit beta 1, is a key component of the extracellular matrix. Laminin, consisting of one α-, one β-, and one γ-chain, is responsible for bridging the internal and external environment of cells and transmitting signals. LAMB1-related genes are enriched in pathways like PI3K-Akt signaling, focal adhesion, and ECM-receptor interaction [1,3].

In mice, knockdown of LAMB1 in the anterior cingulate cortex (ACC) exacerbated pain sensitivity and induced anxiety and depression. Loss of LAMB1 caused actin dysregulation via interaction with integrin β1 and the subsequent Src-dependent RhoA/LIMK/cofilin pathway, leading to abnormal synaptic plasticity and resulting in pain hypersensitivity and anxiodepression-like behaviors [2]. In a study on fracture healing, knockdown of Lamb1 in endothelial cells was detrimental to cell proliferation, migration, and tube formation, and suppressed the expression of genes related to the Wnt/β-catenin signaling pathway, suggesting that Lamb1 promotes fracture repair through this pathway [4].

In conclusion, LAMB1 plays important roles in multiple biological processes. Its functions in pain sensitivity, anxiodepression-like behaviors, and fracture healing have been revealed through loss-of-function experiments in mice. These findings contribute to understanding the role of LAMB1 in related disease areas, such as neuropathic pain and associated psychiatric disorders, as well as bone repair mechanisms.