CORRECTION article
Front. Pharmacol.
Sec. Gastrointestinal and Hepatic Pharmacology
Volume 16 - 2025 | doi: 10.3389/fphar.2025.1633575
Correction: Exploring the lutein therapeutic potential in steatotic liver disease: mechanistic insights and future directions
Provisionally accepted- 1Center for Biomedical Research, Finis Terrae University, Santiago, Chile
- 2Department of Gastroenterology, Faculty of Medicine, Pontificia Universidad Catolica de Chile, Santiago, Chile
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When the original text contained incorrect information, to preserve the scientific record, please include that text when editing the below templates. For example:There was a mistake in the Funding statement, an incorrect number was used. The correct number is '2015C03Bd051'. The publisher apologizes for this mistake.The original version of this article has been updated.In the published article, there was a mistake in the Funding statement. The funding statement for the Key Development Project of the Department of Science and Technology was displayed as '2015CBd051'. The correct statement is 'Key Development Project of Department of Science and Technology (2015C03Bd051)'.Figure 2: Proposed mechanisms involved in lutein-mediated hepatoprotective effects. We propose that independent of its antioxidant and antiapoptotic activity, lutein stimulates LD autophagy in the liver, reducing their accumulation and improving steatosis. This action is mediated through the activation of TFEB. Given lutein's hydrophobic nature as a carotenoid, an intracellular transporter is required to exert its activity within the cell. We propose that STARD3 serves as this transporter. 1) To enter the cell, lutein in lipoproteins, primarily QM and HDL, binds to their transporters on the hepatocyte membrane (SRBI, LDLR, LRP1). 2) Additionally, lutein may directly enter the cell by binding to STARD3 on the plasma membrane. 3) Once inside the cell, lutein bound to STARD3 would directly or indirectly interact with TFEB, mediating its activation. 4) Another pathway for lutein entry involves endosomal uptake, where it binds to STARD3 in the lysosome, activating TFEB via the MCOLN1/Ca2+/calcineurina pathway.End of template. If you would like to request a correction for a reason not seen here, please contact the journal's editorial office.
Keywords: StARD3, TFEB, Hepatic Steatosis, lipid droplet, Lipophagy, Lutein
Received: 23 May 2025; Accepted: 12 Jun 2025.
Copyright: © 2025 Balboa, Saud, Parra-Ruiz, De La Fuente, Landskron and Zanlungo. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Elisa Balboa, Center for Biomedical Research, Finis Terrae University, Santiago, Chile
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