Entrecruzamiento de Colágeno y Resistencia a la Degradación: Análisis Fisiopatológico de la Ineficacia Clínica de los Anticuerpos Anti-LOXL2

DOI: https://doi.org/10.46296/gt.v9i18.0404 Abstract Liver cirrhosis is a progressive disease characterized by the accumulation of extracellular matrix and collagen. The LOXL2 enzyme contributes to the stabilization of fibrosis, and although its inhibition has shown favorable results in murine models, it has not demonstrated significant clinical benefits in humans. A narrative review was conducted using the SALSA framework, analyzing 28 articles published between 2020 and 2026, obtained from PubMed/MEDLINE and Google Scholar. The sources were selected, assessed, and synthesized according to their relevance. Liver fibrosis results from a complex interaction between inflammation, cell death, and extracellular matrix accumulation. The failure of anti-LOXL2 antibodies is related to differences between murine and human models, especially in the immune response, enzyme activity, and characteristics of the fibrotic matrix. Therefore, isolated inhibition of LOXL2 is insufficient, making it necessary to develop combined strategies that promote fibrosis degradation and modulate the hepatic microenvironment. This review analyzes the causes of this discrepancy. Keywords: Liver cirrhosis, experimental fibrosis, lysyl oxidase 2, antifibrotic therapy, murine model.