YKL-40 shows promise as a biomarker for enhancing cardiovascular risk prediction and individualized perioperative decision-making in liver transplantation.
Cardiovascular complications remain a leading cause of morbidity and mortality in liver transplantation (LT), exposing the limitations of current risk assessment strategies. YKL-40, a glycoprotein involved in inflammation, endothelial dysfunction, and fibrotic remodeling, has emerged as a biomarker associated with adverse cardiovascular outcomes and liver disease severity. Its inclusion in structured cardiovascular assessment frameworks may improve transplant-specific risk scores and support earlier identification of high-risk LT recipients. Mechanistically, YKL-40 contributes to vascular injury and myocardial dysfunction via nuclear factor-κB and STAT3 signaling, and is under investigation as a biomarker in preclinical studies aimed at cardiovascular risk modulation in LT. Integration of YKL-40 into predictive models, particularly those supported by artificial intelligence, may enhance individualized perioperative decision-making. This editorial outlines translational directions for integrating YKL-40 into cardiovascular risk models and therapeutic research, supporting its clinical adoption in precision-guided LT care.
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Lulić et al. (2025) studied this question.
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