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Tactics with Prebiotics for the Treatment of Metabolic Dysfunction-Associated Fatty Liver Disease via the Improvement of Mitophagy

Mitophagy/autophagy plays a protective role in various forms of liver damage, by renovating cellular metabolism linking to sustain liver homeostasis. A characterized pathway for mitophagy is the phosphatase and tensin homolog (PTEN)-induced putative kinase 1 (PINK1)/Parkin-dependent signaling pathwa...

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Autores principales: Tsuji, Ai, Yoshikawa, Sayuri, Ikeda, Yuka, Taniguchi, Kurumi, Sawamura, Haruka, Morikawa, Sae, Nakashima, Moeka, Asai, Tomoko, Matsuda, Satoru
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10049478/
https://www.ncbi.nlm.nih.gov/pubmed/36982539
http://dx.doi.org/10.3390/ijms24065465
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author Tsuji, Ai
Yoshikawa, Sayuri
Ikeda, Yuka
Taniguchi, Kurumi
Sawamura, Haruka
Morikawa, Sae
Nakashima, Moeka
Asai, Tomoko
Matsuda, Satoru
author_facet Tsuji, Ai
Yoshikawa, Sayuri
Ikeda, Yuka
Taniguchi, Kurumi
Sawamura, Haruka
Morikawa, Sae
Nakashima, Moeka
Asai, Tomoko
Matsuda, Satoru
author_sort Tsuji, Ai
collection PubMed
description Mitophagy/autophagy plays a protective role in various forms of liver damage, by renovating cellular metabolism linking to sustain liver homeostasis. A characterized pathway for mitophagy is the phosphatase and tensin homolog (PTEN)-induced putative kinase 1 (PINK1)/Parkin-dependent signaling pathway. In particular, PINK1-mediated mitophagy could play an indispensable role in improving the metabolic dysfunction-associated fatty liver disease (MAFLD) which could precede to steatohepatitis (NASH), fibrosis, and hepatocellular carcinoma. In addition, the PI3K/AKT/mTOR pathway might regulate the various characteristics of cellular homeostasis including energy metabolism, cell proliferation, and/or cell protection. Therefore, targeting mitophagy with the alteration of PI3K/AKT/mTOR or PINK1/Parkin-dependent signaling to eliminate impaired mitochondria might be an attractive strategy for the treatment of MAFLD. In particular, the efficacy of prebiotics for the treatment of MAFLD has been suggested to be useful via the modulation of the PI3K/AKT/mTOR/AMPK pathway. Additionally, several edible phytochemicals could activate mitophagy for the improvement of mitochondrial damages, which could also be a promising option to treat MAFLD with providing liver protection. Here, the potential therapeutics with several phytochemicals has been discussed for the treatment of MAFLD. Tactics with a viewpoint of prospective probiotics might contribute to the development of therapeutic interventions.
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spelling pubmed-100494782023-03-29 Tactics with Prebiotics for the Treatment of Metabolic Dysfunction-Associated Fatty Liver Disease via the Improvement of Mitophagy Tsuji, Ai Yoshikawa, Sayuri Ikeda, Yuka Taniguchi, Kurumi Sawamura, Haruka Morikawa, Sae Nakashima, Moeka Asai, Tomoko Matsuda, Satoru Int J Mol Sci Review Mitophagy/autophagy plays a protective role in various forms of liver damage, by renovating cellular metabolism linking to sustain liver homeostasis. A characterized pathway for mitophagy is the phosphatase and tensin homolog (PTEN)-induced putative kinase 1 (PINK1)/Parkin-dependent signaling pathway. In particular, PINK1-mediated mitophagy could play an indispensable role in improving the metabolic dysfunction-associated fatty liver disease (MAFLD) which could precede to steatohepatitis (NASH), fibrosis, and hepatocellular carcinoma. In addition, the PI3K/AKT/mTOR pathway might regulate the various characteristics of cellular homeostasis including energy metabolism, cell proliferation, and/or cell protection. Therefore, targeting mitophagy with the alteration of PI3K/AKT/mTOR or PINK1/Parkin-dependent signaling to eliminate impaired mitochondria might be an attractive strategy for the treatment of MAFLD. In particular, the efficacy of prebiotics for the treatment of MAFLD has been suggested to be useful via the modulation of the PI3K/AKT/mTOR/AMPK pathway. Additionally, several edible phytochemicals could activate mitophagy for the improvement of mitochondrial damages, which could also be a promising option to treat MAFLD with providing liver protection. Here, the potential therapeutics with several phytochemicals has been discussed for the treatment of MAFLD. Tactics with a viewpoint of prospective probiotics might contribute to the development of therapeutic interventions. MDPI 2023-03-13 /pmc/articles/PMC10049478/ /pubmed/36982539 http://dx.doi.org/10.3390/ijms24065465 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Tsuji, Ai
Yoshikawa, Sayuri
Ikeda, Yuka
Taniguchi, Kurumi
Sawamura, Haruka
Morikawa, Sae
Nakashima, Moeka
Asai, Tomoko
Matsuda, Satoru
Tactics with Prebiotics for the Treatment of Metabolic Dysfunction-Associated Fatty Liver Disease via the Improvement of Mitophagy
title Tactics with Prebiotics for the Treatment of Metabolic Dysfunction-Associated Fatty Liver Disease via the Improvement of Mitophagy
title_full Tactics with Prebiotics for the Treatment of Metabolic Dysfunction-Associated Fatty Liver Disease via the Improvement of Mitophagy
title_fullStr Tactics with Prebiotics for the Treatment of Metabolic Dysfunction-Associated Fatty Liver Disease via the Improvement of Mitophagy
title_full_unstemmed Tactics with Prebiotics for the Treatment of Metabolic Dysfunction-Associated Fatty Liver Disease via the Improvement of Mitophagy
title_short Tactics with Prebiotics for the Treatment of Metabolic Dysfunction-Associated Fatty Liver Disease via the Improvement of Mitophagy
title_sort tactics with prebiotics for the treatment of metabolic dysfunction-associated fatty liver disease via the improvement of mitophagy
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10049478/
https://www.ncbi.nlm.nih.gov/pubmed/36982539
http://dx.doi.org/10.3390/ijms24065465
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