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Metabolic dysfunction-associated steatotic liver disease: a key factor in hepatocellular carcinoma therapy response

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Metab Target Organ Damage 2024;4:[Accepted].
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Abstract

The conceptual evolution of non-alcoholic fatty liver disease (NAFLD) to what, since 2023, is called metabolic dysfunction-associated steatotic liver disease (MASLD) not only represents a change in the classification and definition of the disease but also reflects a broader understanding of this heterogeneous condition, which still with many aspects to refine. Although the definition of NAFLD can be interchanged to a high percentage with the new MASLD concept in different aspects, MASLD has been proposed as a relevant factor that influences the response to new immunotherapeutic treatments in the management of MASLD-related hepatocellular carcinoma (HCC), compared to HCC of other etiologies. This indicates that the etiology of HCC plays a relevant role in the prognosis, highlighting the urgency of evaluating treatment regimens for this subgroup of patients in upcoming clinical trials. A better understanding of the pathophysiology of MASLD generates strategies not only aids in its management but also provides strategies to directly intervene in the carcinogenesis of HCC.

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Hepatocellular carcinoma, NAFLD, MASLD, HCC therapy, immunotherapy

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Llamoza-Torres CJ, Fuentes-Pardo M, Ramos-Molina B. Metabolic dysfunction-associated steatotic liver disease: a key factor in hepatocellular carcinoma therapy response. Metab Target Organ Damage 2024;4:[Accept]. http://dx.doi.org/10.20517/mtod.2024.64

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© The Author(s) 2024. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
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Metabolism and Target Organ Damage
ISSN 2769-6375 (Online)
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