Lox, short for Lysyl Oxidase, is a Cu-dependent enzyme. It plays a primary catalytic role in the assembly of the extracellular matrix (ECM), which is crucial for cell fate, differentiation, and communication during development, tissue maintenance, and repair [2]. It is involved in multiple signaling pathways, such as those related to EGFR, PDGF, VEGF, TGF-β, mechano-transduction, inflammatory, and steroid signaling [2].

In animal models, LOX-1 knockout mice exhibit reduced intima thickness and inflammation, along with increased expression of protective factors, indicating its key role in atherogenic processes [1]. In hypoxic-ischemic brain damage, elevated LOX expression correlates with the severity of hypoxic-ischemic encephalopathy (HIE). Pharmacological inhibition of LOX ameliorates brain neuronal ferroptosis and improves learning and memory impairments [3].

In conclusion, Lox is essential for ECM assembly and participates in various signaling pathways. Gene knockout models in mice have revealed its significance in atherosclerosis and hypoxic-ischemic brain damage, providing insights into potential therapeutic targets for these diseases.