Laptm4b, short for lysosomal-associated transmembrane protein 4B, is a protein-coding gene. It is involved in multiple biological processes, including the regulation of autophagic flux, cell proliferation, invasion, metastasis, apoptosis resistance, autophagy initiation, and drug resistance. It has connections with pathways such as mTORC1, PI3K/AKT, and is also associated with the regulation of ferroptosis. Genetic models, like knockout mouse models, have been crucial in understanding its functions [1-3, 5].

In myocardial ischemia/reperfusion injury, Laptm4b-knockout (Laptm4b-/ -) mice had increased infarct size and lactate dehydrogenase release. The down-regulation of Laptm4b led to impaired autophagic flux via unopposed activation of mTORC1 signaling [1]. In various cancers, Laptm4b-knockdown inhibited cell proliferation, invasion, and metastasis. For example, in acute myeloid leukemia (AML), Laptm4b promoted leukemia progression, and its knockdown could potentially target AML treatment [2]. In non-small cell lung cancer, Laptm4b knockout affected the metabolic landscape, leading to an enrichment of ferroptosis-associated metabolic alterations [3].

In conclusion, Laptm4b plays essential roles in autophagic flux regulation and cancer-related biological processes. The use of Laptm4b knockout mouse models has significantly contributed to understanding its functions in myocardial ischemia/reperfusion injury and cancer, providing insights into potential therapeutic targets for these disease areas.