Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/103470
Title: Pomegranate activates TFEB to promote autophagy-lysosomal fitness and mitophagy
Authors: Tan, Sijie
Yu, Chye Yun
Sim, Zhi Wei
Low, Zun Siong
Lee, Brianna
See, Faith
Min, Nyo
Gautam, Archana
Chu, Justin Jang Hann
Ng, Kee Woei
Wong, Esther
Keywords: Cellular Neuroscience
Macroautophagy
DRNTU::Engineering::Materials
Issue Date: 2019
Source: Tan, S., Yu, C. Y., Sim, Z. W., Low, Z. S., Lee, B., See, F., … Wong, E. (2019). Pomegranate activates TFEB to promote autophagy-lysosomal fitness and mitophagy. Scientific Reports, 9(1). doi:10.1038/s41598-018-37400-1
Series/Report no.: Scientific Reports
Abstract: Mitochondrial dysfunction underscores aging and diseases. Mitophagy (mitochondria + autophagy) is a quality control pathway that preserves mitochondrial health by targeting damaged mitochondria for autophagic degradation. Hence, molecules or compounds that can augment mitophagy are therapeutic candidates to mitigate mitochondrial-related diseases. However, mitochondrial stress remains the most effective inducer of mitophagy. Thus, identification of mitophagy-inducing regimes that are clinically relevant is favorable. In this study, pomegranate extract (PE) supplementation is shown to stimulate mitophagy. PE activates transcription factor EB (TFEB) to upregulate the expression of autophagy and lysosomal genes for mitochondrial quality control under basal and stress conditions. Basally, PE alters mitochondrial morphology and promotes recruitment of autophagosomes to the mitochondria (mitophagosome formation). Upon onset of mitochondrial stress, PE further augments mitophagosome formation, and engages PINK1 and Parkin to the mitochondria to potentiate mitophagy. This cellular phenomenon of PE-induced mitophagy helps to negate superfluous mitochondrial reactive oxygen species (ROS) production and mitochondrial impairment. Overall, our study highlights the potential of PE supplementation as a physiological therapy to modulate TFEB activity to alleviate mitochondrial dysfunction in aging and mitochondrial-related diseases.
URI: https://hdl.handle.net/10356/103470
http://hdl.handle.net/10220/48091
DOI: 10.1038/s41598-018-37400-1
Rights: © 2019 The Author(s). 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.
Fulltext Permission: open
Fulltext Availability: With Fulltext
Appears in Collections:MSE Journal Articles
SBS Journal Articles

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