Nicotinamide riboside promotes autolysosome clearance in preventing doxorubicin-induced cardiotoxicity
Identifieur interne : 000757 ( Ncbi/Checkpoint ); précédent : 000756; suivant : 000758Nicotinamide riboside promotes autolysosome clearance in preventing doxorubicin-induced cardiotoxicity
Auteurs : Dong Zheng [République populaire de Chine, Canada] ; Yi Zhang [République populaire de Chine] ; Ming Zheng [République populaire de Chine] ; Ting Cao [République populaire de Chine] ; Grace Wang [Canada] ; Lulu Zhang [République populaire de Chine] ; Rui Ni [Canada] ; Joseph Brockman [Canada] ; Huiting Zhong [République populaire de Chine] ; Guo-Chang Fan [États-Unis] ; Tianqing Peng [République populaire de Chine, Canada]Source :
- Clinical science (London, England : 1979) [ 0143-5221 ] ; 2019.
Abstract
Doxorubicin (DOX) is widely used as a first-line chemotherapeutic drug for various malignancies. However, DOX causes severe cardiotoxicity, which limits its clinical uses. Oxidative stress is one of major contributors to DOX-induced cardiotoxicity. While autophagic flux serves as an important defense mechanism against oxidative stress in cardiomyocytes, recent studies have demonstrated that DOX induces the blockage of autophagic flux, which contributes to DOX cardiotoxicity. The present study investigated whether nicotinamide riboside (NR), a precursor of nicotinamide adenine dinucleotide (NAD)+, prevents DOX cardiotoxicity by improving autophagic flux. We report that administration of NR elevated NAD+ levels, and reduced cardiac injury and myocardial dysfunction in DOX-injected mice. These protective effects of NR were recapitulated in cultured cardiomyocytes upon DOX treatment. Mechanistically, NR prevented the blockage of autophagic flux, accumulation of autolysosomes, and oxidative stress in DOX-treated cardiomyocytes, the effects of which were associated with restoration of lysosomal acidification. Furthermore, inhibition of lysosomal acidification or SIRT1 abrogated these protective effects of NR during DOX-induced cardiotoxicity. Collectively, our study shows that NR enhances autolysosome clearance via the NAD+/SIRT1 signaling, thereby preventing DOX-triggered cardiotoxicity.
Url:
DOI: 10.1042/CS20181022
PubMed: 31266854
PubMed Central: 6705112
Affiliations:
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4S2;</nlm:aff><country>Canada</country><wicri:regionArea>Critical Illness Research, Lawson Health Research Institute, London Health Sciences Centre, VRL 6th Floor, A6-140, 800 Commissioners Road, London, ON</wicri:regionArea><wicri:noRegion>ON</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="A3">Departments of Medicine and Pathology and Laboratory Medicine, Western University, London, ON, Canada N6A 4S2;</nlm:aff><country>Canada</country><wicri:regionArea>Departments of Medicine and Pathology and Laboratory Medicine, Western University, London, ON</wicri:regionArea><wicri:noRegion>ON</wicri:noRegion></affiliation></author><author><name sortKey="Zhang, Yi" sort="Zhang, Yi" uniqKey="Zhang Y" first="Yi" last="Zhang">Yi Zhang</name><affiliation wicri:level="1"><nlm:aff id="A1">Institutes of Biology and Medical Sciences, Soochow University, Suzhou 215123, China;</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Institutes of Biology and Medical Sciences, Soochow University, Suzhou 215123</wicri:regionArea><wicri:noRegion>Suzhou 215123</wicri:noRegion></affiliation></author><author><name sortKey="Zheng, Ming" sort="Zheng, Ming" uniqKey="Zheng M" first="Ming" last="Zheng">Ming Zheng</name><affiliation wicri:level="1"><nlm:aff id="A1">Institutes of Biology and Medical Sciences, Soochow University, Suzhou 215123, China;</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Institutes of Biology and Medical Sciences, Soochow University, Suzhou 215123</wicri:regionArea><wicri:noRegion>Suzhou 215123</wicri:noRegion></affiliation></author><author><name sortKey="Cao, Ting" sort="Cao, Ting" uniqKey="Cao T" first="Ting" last="Cao">Ting Cao</name><affiliation wicri:level="1"><nlm:aff id="A1">Institutes of Biology and Medical Sciences, Soochow University, Suzhou 215123, China;</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Institutes of Biology and Medical Sciences, Soochow University, Suzhou 215123</wicri:regionArea><wicri:noRegion>Suzhou 215123</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Grace" sort="Wang, Grace" uniqKey="Wang G" first="Grace" last="Wang">Grace Wang</name><affiliation wicri:level="4"><nlm:aff id="A4">Faculty of Medicine, University of Toronto, 1 King’s College Circle, Toronto, ON, Canada M5S 1A8;</nlm:aff><country>Canada</country><wicri:regionArea>Faculty of Medicine, University of Toronto, 1 King’s College Circle, Toronto, ON</wicri:regionArea><orgName type="university">Université de Toronto</orgName><placeName><settlement type="city">Toronto</settlement><region type="state">Ontario</region></placeName></affiliation></author><author><name sortKey="Zhang, Lulu" sort="Zhang, Lulu" uniqKey="Zhang L" first="Lulu" last="Zhang">Lulu Zhang</name><affiliation wicri:level="1"><nlm:aff id="A1">Institutes of Biology and Medical Sciences, Soochow University, Suzhou 215123, China;</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Institutes of Biology and Medical Sciences, Soochow University, Suzhou 215123</wicri:regionArea><wicri:noRegion>Suzhou 215123</wicri:noRegion></affiliation></author><author><name sortKey="Ni, Rui" sort="Ni, Rui" uniqKey="Ni R" first="Rui" last="Ni">Rui Ni</name><affiliation wicri:level="1"><nlm:aff id="A2">Critical Illness Research, Lawson Health Research Institute, London Health Sciences Centre, VRL 6th Floor, A6-140, 800 Commissioners Road, London, ON, Canada N6A 4S2;</nlm:aff><country>Canada</country><wicri:regionArea>Critical Illness Research, Lawson Health Research Institute, London Health Sciences Centre, VRL 6th Floor, A6-140, 800 Commissioners Road, London, ON</wicri:regionArea><wicri:noRegion>ON</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="A3">Departments of Medicine and Pathology and Laboratory Medicine, Western University, London, ON, Canada N6A 4S2;</nlm:aff><country>Canada</country><wicri:regionArea>Departments of Medicine and Pathology and Laboratory Medicine, Western University, London, ON</wicri:regionArea><wicri:noRegion>ON</wicri:noRegion></affiliation></author><author><name sortKey="Brockman, Joseph" sort="Brockman, Joseph" uniqKey="Brockman J" first="Joseph" last="Brockman">Joseph Brockman</name><affiliation wicri:level="1"><nlm:aff id="A3">Departments of Medicine and Pathology and Laboratory Medicine, Western University, London, ON, Canada N6A 4S2;</nlm:aff><country>Canada</country><wicri:regionArea>Departments of Medicine and Pathology and Laboratory Medicine, Western University, London, ON</wicri:regionArea><wicri:noRegion>ON</wicri:noRegion></affiliation></author><author><name sortKey="Zhong, Huiting" sort="Zhong, Huiting" uniqKey="Zhong H" first="Huiting" last="Zhong">Huiting Zhong</name><affiliation wicri:level="1"><nlm:aff id="A1">Institutes of Biology and Medical Sciences, Soochow University, Suzhou 215123, China;</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Institutes of Biology and Medical Sciences, Soochow University, Suzhou 215123</wicri:regionArea><wicri:noRegion>Suzhou 215123</wicri:noRegion></affiliation></author><author><name sortKey="Fan, Guo Chang" sort="Fan, Guo Chang" uniqKey="Fan G" first="Guo-Chang" last="Fan">Guo-Chang Fan</name><affiliation wicri:level="1"><nlm:aff id="A5">Department of Pharmacology and Systems Physiology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, U.S.A.</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pharmacology and Systems Physiology, University of Cincinnati College of Medicine, Cincinnati, OH 45267</wicri:regionArea><wicri:noRegion>OH 45267</wicri:noRegion></affiliation></author><author><name sortKey="Peng, Tianqing" sort="Peng, Tianqing" uniqKey="Peng T" first="Tianqing" last="Peng">Tianqing Peng</name><affiliation wicri:level="1"><nlm:aff id="A1">Institutes of Biology and Medical Sciences, Soochow University, Suzhou 215123, China;</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Institutes of Biology and Medical Sciences, Soochow University, Suzhou 215123</wicri:regionArea><wicri:noRegion>Suzhou 215123</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="A2">Critical Illness Research, Lawson Health Research Institute, London Health Sciences Centre, VRL 6th Floor, A6-140, 800 Commissioners Road, London, ON, Canada N6A 4S2;</nlm:aff><country>Canada</country><wicri:regionArea>Critical Illness Research, Lawson Health Research Institute, London Health Sciences Centre, VRL 6th Floor, A6-140, 800 Commissioners Road, London, ON</wicri:regionArea><wicri:noRegion>ON</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="A3">Departments of Medicine and Pathology and Laboratory Medicine, Western University, London, ON, Canada N6A 4S2;</nlm:aff><country>Canada</country><wicri:regionArea>Departments of Medicine and Pathology and Laboratory Medicine, Western University, London, ON</wicri:regionArea><wicri:noRegion>ON</wicri:noRegion></affiliation></author></analytic><series><title level="j">Clinical science (London, England : 1979)</title><idno type="ISSN">0143-5221</idno><idno type="eISSN">1470-8736</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P4">Doxorubicin (DOX) is widely used as a first-line chemotherapeutic drug for various malignancies. However, DOX causes severe cardiotoxicity, which limits its clinical uses. Oxidative stress is one of major contributors to DOX-induced cardiotoxicity. While autophagic flux serves as an important defense mechanism against oxidative stress in cardiomyocytes, recent studies have demonstrated that DOX induces the blockage of autophagic flux, which contributes to DOX cardiotoxicity. The present study investigated whether nicotinamide riboside (NR), a precursor of nicotinamide adenine dinucleotide (NAD)<sup>+</sup>, prevents DOX cardiotoxicity by improving autophagic flux. We report that administration of NR elevated NAD<sup>+</sup> levels, and reduced cardiac injury and myocardial dysfunction in DOX-injected mice. These protective effects of NR were recapitulated in cultured cardiomyocytes upon DOX treatment. Mechanistically, NR prevented the blockage of autophagic flux, accumulation of autolysosomes, and oxidative stress in DOX-treated cardiomyocytes, the effects of which were associated with restoration of lysosomal acidification. Furthermore, inhibition of lysosomal acidification or SIRT1 abrogated these protective effects of NR during DOX-induced cardiotoxicity. Collectively, our study shows that NR enhances autolysosome clearance via the NAD<sup>+</sup>/SIRT1 signaling, thereby preventing DOX-triggered cardiotoxicity.</p></div></front></TEI><affiliations><list><country><li>Canada</li><li>République populaire de Chine</li><li>États-Unis</li></country><region><li>Ontario</li></region><settlement><li>Toronto</li></settlement><orgName><li>Université de Toronto</li></orgName></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Zheng, Dong" sort="Zheng, Dong" uniqKey="Zheng D" first="Dong" last="Zheng">Dong Zheng</name></noRegion><name sortKey="Cao, Ting" sort="Cao, Ting" uniqKey="Cao T" first="Ting" last="Cao">Ting Cao</name><name sortKey="Peng, Tianqing" sort="Peng, Tianqing" uniqKey="Peng T" first="Tianqing" last="Peng">Tianqing Peng</name><name sortKey="Zhang, Lulu" sort="Zhang, Lulu" uniqKey="Zhang L" first="Lulu" last="Zhang">Lulu Zhang</name><name sortKey="Zhang, Yi" sort="Zhang, Yi" uniqKey="Zhang Y" first="Yi" last="Zhang">Yi Zhang</name><name sortKey="Zheng, Ming" sort="Zheng, Ming" uniqKey="Zheng M" first="Ming" last="Zheng">Ming Zheng</name><name sortKey="Zhong, Huiting" sort="Zhong, Huiting" uniqKey="Zhong H" first="Huiting" last="Zhong">Huiting Zhong</name></country><country name="Canada"><noRegion><name sortKey="Zheng, Dong" sort="Zheng, Dong" uniqKey="Zheng D" first="Dong" last="Zheng">Dong Zheng</name></noRegion><name sortKey="Brockman, Joseph" sort="Brockman, Joseph" uniqKey="Brockman J" first="Joseph" last="Brockman">Joseph Brockman</name><name sortKey="Ni, Rui" sort="Ni, Rui" uniqKey="Ni R" first="Rui" last="Ni">Rui Ni</name><name sortKey="Ni, Rui" sort="Ni, Rui" uniqKey="Ni R" first="Rui" last="Ni">Rui Ni</name><name sortKey="Peng, Tianqing" sort="Peng, Tianqing" uniqKey="Peng T" first="Tianqing" last="Peng">Tianqing Peng</name><name sortKey="Peng, Tianqing" sort="Peng, Tianqing" uniqKey="Peng T" first="Tianqing" last="Peng">Tianqing Peng</name><name sortKey="Wang, Grace" sort="Wang, Grace" uniqKey="Wang G" first="Grace" last="Wang">Grace Wang</name><name sortKey="Zheng, Dong" sort="Zheng, Dong" uniqKey="Zheng D" first="Dong" last="Zheng">Dong Zheng</name></country><country name="États-Unis"><noRegion><name sortKey="Fan, Guo Chang" sort="Fan, Guo Chang" uniqKey="Fan G" first="Guo-Chang" last="Fan">Guo-Chang Fan</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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