Lcp1, also known as Lymphocyte cytosolic protein 1, is an actin-binding protein that facilitates cell migration, immune responses, actin polymerization, cytoskeletal rearrangements, and phagocytosis [1]. It is involved in multiple signaling pathways, such as Akt, EGFR, JAK2/STAT3, and mTORC2/AKT, and is crucial for various biological processes [1,3,4]. Genetic models, like knockout mice, are valuable for studying Lcp1's functions.

In a mouse model of ischemic stroke, knockdown of Lcp1 in monocyte-derived macrophages reduced ischemic infarction, improved neurological behaviors, decreased neuroinflammation, and attenuated lymphopenia. It also altered immune cell signaling and metabolism, with Lcp1high monocytes/macrophages showing enrichment in fatty acid and glycolysis metabolism, as well as enhanced oxidative phosphorylation, chemotaxis, migration, and ATP biosynthesis pathways [1].

In an osteoarthritis mouse model, Lcp1 knockout suppressed subchondral osteoclasts, decreased bone remodeling, retarded cartilage degeneration, and maintained a hypoxic environment in joints [2].

In conclusion, Lcp1 plays essential roles in cell migration, immune responses, and metabolism. Gene-knockout mouse models have revealed its significance in ischemic stroke and osteoarthritis. Understanding Lcp1 functions can potentially lead to new therapeutic strategies for these and other related diseases.