Autophagy in metabolic syndrome: breaking the wheel by targeting the renin–angiotensin system
Identifieur interne : 000207 ( an2020/Analysis ); précédent : 000206; suivant : 000208Autophagy in metabolic syndrome: breaking the wheel by targeting the renin–angiotensin system
Auteurs : Kalhara R. Menikdiwela [États-Unis] ; Latha Ramalingam [États-Unis] ; Fahmida Rasha [États-Unis] ; Shu Wang [États-Unis] ; Jannette M. Dufour [États-Unis] ; Nishan S. Kalupahana [États-Unis, Sri Lanka] ; Karen K. S. Sunahara [Brésil] ; Joilson O. Martins [Brésil] ; Naima Moustaid-Moussa [États-Unis]Source :
- Cell Death & Disease [ 2041-4889 ] ; 2020.
Abstract
Metabolic syndrome (MetS) is a complex, emerging epidemic which disrupts the metabolic homeostasis of several organs, including liver, heart, pancreas, and adipose tissue. While studies have been conducted in these research areas, the pathogenesis and mechanisms of MetS remain debatable. Lines of evidence show that physiological systems, such as the renin–angiotensin system (RAS) and autophagy play vital regulatory roles in MetS. RAS is a pivotal system known for controlling blood pressure and fluid balance, whereas autophagy is involved in the degradation and recycling of cellular components, including proteins. Although RAS is activated in MetS, the interrelationship between RAS and autophagy varies in glucose homeostatic organs and their cross talk is poorly understood. Interestingly, autophagy is attenuated in the liver during MetS, whereas autophagic activity is induced in adipose tissue during MetS, indicating tissue-specific discordant roles. We discuss in vivo and in vitro studies conducted in metabolic tissues and dissect their tissue-specific effects. Moreover, our review will focus on the molecular mechanisms by which autophagy orchestrates MetS and the ways future treatments could target RAS in order to achieve metabolic homeostasis.
Url:
DOI: 10.1038/s41419-020-2275-9
PubMed: 32015340
PubMed Central: 6997396
Affiliations:
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PMC:6997396Le document en format XML
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S." last="Sunahara">Karen K. S. Sunahara</name><affiliation wicri:level="1"><nlm:aff id="Aff5"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1937 0722</institution-id><institution-id institution-id-type="GRID">grid.11899.38</institution-id><institution>Department of Experimental Physiopatholgy,</institution><institution>Medical School University of São Paulo,</institution></institution-wrap>São Paulo, Brazil</nlm:aff><country xml:lang="fr">Brésil</country><wicri:regionArea>São Paulo</wicri:regionArea></affiliation></author><author><name sortKey="Martins, Joilson O" sort="Martins, Joilson O" uniqKey="Martins J" first="Joilson O." last="Martins">Joilson O. Martins</name><affiliation wicri:level="1"><nlm:aff id="Aff6"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1937 0722</institution-id><institution-id institution-id-type="GRID">grid.11899.38</institution-id><institution>Laboratory of Immunoendocrinology, Department of Clinical and Toxicological Analyses,</institution><institution>School of Pharmaceutical Sciences of University Sao Paulo (FCF/USP),</institution></institution-wrap>São Paulo, Brazil</nlm:aff><country xml:lang="fr">Brésil</country><wicri:regionArea>São Paulo</wicri:regionArea></affiliation></author><author><name sortKey="Moustaid Moussa, Naima" sort="Moustaid Moussa, Naima" uniqKey="Moustaid Moussa N" first="Naima" last="Moustaid-Moussa">Naima Moustaid-Moussa</name><affiliation wicri:level="2"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2186 7496</institution-id><institution-id institution-id-type="GRID">grid.264784.b</institution-id><institution>Department of Nutritional Sciences,</institution><institution>Texas Tech University,</institution></institution-wrap>Lubbock, TX USA</nlm:aff><country>États-Unis</country><placeName><region type="state">Texas</region></placeName><wicri:cityArea>Lubbock</wicri:cityArea></affiliation><affiliation wicri:level="2"><nlm:aff id="Aff2"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2186 7496</institution-id><institution-id institution-id-type="GRID">grid.264784.b</institution-id><institution>Obesity Research Institute,</institution><institution>Texas Tech University,</institution></institution-wrap>Lubbock, TX USA</nlm:aff><country>États-Unis</country><placeName><region type="state">Texas</region></placeName><wicri:cityArea>Lubbock</wicri:cityArea></affiliation></author></analytic><series><title level="j">Cell Death & Disease</title><idno type="eISSN">2041-4889</idno><imprint><date when="2020">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="Par1">Metabolic syndrome (MetS) is a complex, emerging epidemic which disrupts the metabolic homeostasis of several organs, including liver, heart, pancreas, and adipose tissue. While studies have been conducted in these research areas, the pathogenesis and mechanisms of MetS remain debatable. Lines of evidence show that physiological systems, such as the renin–angiotensin system (RAS) and autophagy play vital regulatory roles in MetS. RAS is a pivotal system known for controlling blood pressure and fluid balance, whereas autophagy is involved in the degradation and recycling of cellular components, including proteins. Although RAS is activated in MetS, the interrelationship between RAS and autophagy varies in glucose homeostatic organs and their cross talk is poorly understood. Interestingly, autophagy is attenuated in the liver during MetS, whereas autophagic activity is induced in adipose tissue during MetS, indicating tissue-specific discordant roles. We discuss in vivo and in vitro studies conducted in metabolic tissues and dissect their tissue-specific effects. 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Menikdiwela</name></region><name sortKey="Dufour, Jannette M" sort="Dufour, Jannette M" uniqKey="Dufour J" first="Jannette M." last="Dufour">Jannette M. Dufour</name><name sortKey="Dufour, Jannette M" sort="Dufour, Jannette M" uniqKey="Dufour J" first="Jannette M." last="Dufour">Jannette M. Dufour</name><name sortKey="Kalupahana, Nishan S" sort="Kalupahana, Nishan S" uniqKey="Kalupahana N" first="Nishan S." last="Kalupahana">Nishan S. Kalupahana</name><name sortKey="Kalupahana, Nishan S" sort="Kalupahana, Nishan S" uniqKey="Kalupahana N" first="Nishan S." last="Kalupahana">Nishan S. Kalupahana</name><name sortKey="Menikdiwela, Kalhara R" sort="Menikdiwela, Kalhara R" uniqKey="Menikdiwela K" first="Kalhara R." last="Menikdiwela">Kalhara R. Menikdiwela</name><name sortKey="Moustaid Moussa, Naima" sort="Moustaid Moussa, Naima" uniqKey="Moustaid Moussa N" first="Naima" last="Moustaid-Moussa">Naima Moustaid-Moussa</name><name sortKey="Moustaid Moussa, Naima" sort="Moustaid Moussa, Naima" uniqKey="Moustaid Moussa N" first="Naima" last="Moustaid-Moussa">Naima Moustaid-Moussa</name><name sortKey="Ramalingam, Latha" sort="Ramalingam, Latha" uniqKey="Ramalingam L" first="Latha" last="Ramalingam">Latha Ramalingam</name><name sortKey="Ramalingam, Latha" sort="Ramalingam, Latha" uniqKey="Ramalingam L" first="Latha" last="Ramalingam">Latha Ramalingam</name><name sortKey="Rasha, Fahmida" sort="Rasha, Fahmida" uniqKey="Rasha F" first="Fahmida" last="Rasha">Fahmida Rasha</name><name sortKey="Rasha, Fahmida" sort="Rasha, Fahmida" uniqKey="Rasha F" first="Fahmida" last="Rasha">Fahmida Rasha</name><name sortKey="Wang, Shu" sort="Wang, Shu" uniqKey="Wang S" first="Shu" last="Wang">Shu Wang</name><name sortKey="Wang, Shu" sort="Wang, Shu" uniqKey="Wang S" first="Shu" last="Wang">Shu Wang</name></country><country name="Sri Lanka"><noRegion><name sortKey="Kalupahana, Nishan S" sort="Kalupahana, Nishan S" uniqKey="Kalupahana N" first="Nishan S." last="Kalupahana">Nishan S. Kalupahana</name></noRegion></country><country name="Brésil"><noRegion><name sortKey="Sunahara, Karen K S" sort="Sunahara, Karen K S" uniqKey="Sunahara K" first="Karen K. S." last="Sunahara">Karen K. S. Sunahara</name></noRegion><name sortKey="Martins, Joilson O" sort="Martins, Joilson O" uniqKey="Martins J" first="Joilson O." last="Martins">Joilson O. Martins</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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