Please use this identifier to cite or link to this item: https://doi.org/10.1038/s41598-018-37400-1
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: Science & Technology
Multidisciplinary Sciences
Science & Technology - Other Topics
TRANSCRIPTION FACTOR EB
THERAPEUTIC TARGET
OXIDATIVE STRESS
MITOCHONDRIAL
MTOR
PARKIN
BIOGENESIS
CALCIUM
PHOSPHORYLATION
DEGRADATION
Issue Date: 24-Jan-2019
Publisher: NATURE PUBLISHING GROUP
Citation: 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 (2019-01-24). POMEGRANATE ACTIVATES TFEB TO PROMOTE AUTOPHAGY-LYSOSOMAL FITNESS AND MITOPHAGY 9 (1). ScholarBank@NUS Repository. https://doi.org/10.1038/s41598-018-37400-1
Abstract: © 2019, The Author(s). 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://scholarbank.nus.edu.sg/handle/10635/155375
ISSN: 2045-2322
2045-2322
DOI: 10.1038/s41598-018-37400-1
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