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. 2024 Jul 6;14:90. doi: 10.1186/s13578-024-01267-9

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — Drug candidates for MASLD. Pioglitazone and saroglitazar are promising drugs for treating MASLD because they activate PPAR receptors to enhance isulin sensitivity. Empagliflozin inhibits sodium-glucose cotransporter-2 (SGLT-2), which enhances the urinary excretion of glucose to reduce hyperglycemia. Obeticholic acid, EDP-305 and cilofor activate farnesoid X receptor (FXR) to enhance isulin sensitivity. MGL-3196 reduces hepatic lipid accumulation by activating the thyroid hormone receptor (THR). Aramchol inhibits stearoyl-CoA desaturase 1 to alleviate hepatic steatosis. PF-06835919 can inhibit ketohexokinase in the TCA cycle, subsequently controlling fructose metabolism. Pegozafermin enhances insulin sensitivity and fatty acid β-oxidation by activating farnesoid X receptor (FXR) to alleviate MASLD