Fuentes-Mendoza JM, Concepción-Zavaleta MJ, Mendoza-Godoy JJ, Concepción-Urteaga LA, Martínez-Gutiérrez CO, Paz-Ibarra J. Dyslipidemia in liver cirrhosis: Pathophysiology and emerging therapeutic approaches. World J Hepatol 2026; 18(3): 115539 [DOI: 10.4254/wjh.v18.i3.115539]
Corresponding Author of This Article
Marcio J Concepción-Zavaleta, MD, Neuroscience, Metabolism, Clinical and Health Effectiveness Research Group, Universidad Científica del Sur, 19 Panamericana Sur, Villa El Salvador, Lima 15067, Peru. mconcepcion@cientifica.edu.pe
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Minireviews
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This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Hepatol. Mar 27, 2026; 18(3): 115539 Published online Mar 27, 2026. doi: 10.4254/wjh.v18.i3.115539
Dyslipidemia in liver cirrhosis: Pathophysiology and emerging therapeutic approaches
Jenyfer M Fuentes-Mendoza, Marcio J Concepción-Zavaleta, Jeny J Mendoza-Godoy, Luis A Concepción-Urteaga, Carlos O Martínez-Gutiérrez, José Paz-Ibarra
Jenyfer M Fuentes-Mendoza, Marcio J Concepción-Zavaleta, Grupo de Investigación en Neurociencias, Metabolismo, Efectividad Clínica y Salud Pública, Universidad Científica del Sur, Lima 15067, Peru
Jeny J Mendoza-Godoy, School of Medicine, Universidad Privada de Huancayo Franklin Roosevelt, Huancayo 12001, Junín, Peru
Luis A Concepción-Urteaga, School of Medicine, Universidad Nacional de Trujillo, Trujillo 13011, La Libertad, Peru
Carlos O Martínez-Gutiérrez, School of Medicine, Universidad Autónoma de San Luis Potosí, San Luis Potosí 78210, Mexico
José Paz-Ibarra, School of Medicine, Universidad Nacional Mayor de San Marcos, Lima 15081, Peru
José Paz-Ibarra, Division of Endocrinology, Edgardo Rebagliati Martins National Hospital, Lima 15072, Peru
Author contributions: Fuentes-Mendoza JM and Concepción-Zavaleta MJ conceived and designed the review and coordinated the project; Fuentes-Mendoza JM and Mendoza-Godoy JJ performed the literature search, data extraction and synthesis; Fuentes-Mendoza JM and Martínez-Gutiérrez CO drafted the initial manuscript; Concepción-Urteaga LA and Paz-Ibarra J contributed clinical expertise, interpretation of evidence and critical input on safety and therapeutic perspectives. All authors critically revised the manuscript for important intellectual content, approved the final version, and agree to be accountable for all aspects of the work.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Corresponding author: Marcio J Concepción-Zavaleta, MD, Neuroscience, Metabolism, Clinical and Health Effectiveness Research Group, Universidad Científica del Sur, 19 Panamericana Sur, Villa El Salvador, Lima 15067, Peru. mconcepcion@cientifica.edu.pe
Received: October 20, 2025 Revised: November 12, 2025 Accepted: January 21, 2026 Published online: March 27, 2026 Processing time: 158 Days and 6.5 Hours
Core Tip
Core Tip: Dyslipidemia in liver cirrhosis reflects fundamental alterations in hepatic lipid biology, including impaired apolipoprotein synthesis, defective lipoprotein export, receptor downregulation, and cholestasis-driven accumulation of atypical particles such as lipoprotein X and lipoprotein Z. These molecular disturbances generate stage-specific lipid phenotypes that challenge conventional cardiovascular risk assessment and drug targeting. Non-statin lipid-lowering agents provide mechanistically informative tools to probe these disrupted pathways; however, their effects in cirrhosis remain largely defined by pharmacologic rationale rather than direct clinical evidence. Understanding how disease stage and etiology reshape hepatic lipid handling is essential for rational application and future development of lipid-modifying strategies in cirrhotic populations.
