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Abstract Liver fibrosis involves increased extracellular matrix (ECM) deposition, with lysyl oxidase‐like 2 (LOXL2) emerging as a key player due to its upregulation in fibrotic tissue. As a member of the lysyl oxidase protein family, LOXL2 contributes to ECM accumulation and remodelling through fibre cross‐linking. Its aberrant expression in non‐alcoholic steatohepatitis (NASH) implicates it in liver fibrosis. LOXL2 promotes fibrosis by activating hepatic stellate cells, cross‐linking ECM proteins, and influencing oxidative stress, inflammation and lipid metabolism. Preclinical studies on LOXL2 inhibitors show promise in reducing fibrosis and improving liver function. Ongoing clinical trials further highlight LOXL2 as a potential anti‐fibrotic target. However, challenges such as species differences, tissue‐specific effects and the complexity of NASH pathogenesis require additional research. Understanding LOXL2's role in NASH will aid in developing effective treatments for NASH‐related fibrosis and liver damage.
Immanuel et al. (Fri,) studied this question.