Please use this identifier to cite or link to this item: https://doi.org/10.1038/s41598-018-37400-1
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dc.titlePOMEGRANATE ACTIVATES TFEB TO PROMOTE AUTOPHAGY-LYSOSOMAL FITNESS AND MITOPHAGY
dc.contributor.authorTan, Sijie
dc.contributor.authorYu, Chye Yun
dc.contributor.authorSim, Zhi Wei
dc.contributor.authorLow, Zun Siong
dc.contributor.authorLee, Brianna
dc.contributor.authorSee, Faith
dc.contributor.authorMin, Nyo
dc.contributor.authorGautam, Archana
dc.contributor.authorChu, Justin Jang Hann
dc.contributor.authorNg, Kee Woei
dc.contributor.authorWong, Esther
dc.date.accessioned2019-06-07T02:02:45Z
dc.date.available2019-06-07T02:02:45Z
dc.date.issued2019-01-24
dc.identifier.citationTan, 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
dc.identifier.issn2045-2322
dc.identifier.issn2045-2322
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/155375
dc.description.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.
dc.language.isoen
dc.publisherNATURE PUBLISHING GROUP
dc.sourceElements
dc.subjectScience & Technology
dc.subjectMultidisciplinary Sciences
dc.subjectScience & Technology - Other Topics
dc.subjectTRANSCRIPTION FACTOR EB
dc.subjectTHERAPEUTIC TARGET
dc.subjectOXIDATIVE STRESS
dc.subjectMITOCHONDRIAL
dc.subjectMTOR
dc.subjectPARKIN
dc.subjectBIOGENESIS
dc.subjectCALCIUM
dc.subjectPHOSPHORYLATION
dc.subjectDEGRADATION
dc.typeArticle
dc.date.updated2019-06-04T01:59:24Z
dc.contributor.departmentDEPT OF PHYSIOLOGY
dc.contributor.departmentDEPT OF MICROBIOLOGY & IMMUNOLOGY
dc.description.doi10.1038/s41598-018-37400-1
dc.description.volume9
dc.description.issue1
dc.published.statePublished
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