Autophagy in metabolic syndrome: breaking the wheel by targeting the renin–angiotensin system
Identifieur interne : 000223 ( Pmc/Curation ); précédent : 000222; suivant : 000224Autophagy 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
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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>
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<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. 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.</p>
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<front><journal-meta><journal-id journal-id-type="nlm-ta">Cell Death Dis</journal-id>
<journal-id journal-id-type="iso-abbrev">Cell Death Dis</journal-id>
<journal-title-group><journal-title>Cell Death & Disease</journal-title>
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<issn pub-type="epub">2041-4889</issn>
<publisher><publisher-name>Nature Publishing Group UK</publisher-name>
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<article-id pub-id-type="publisher-id">2275</article-id>
<article-id pub-id-type="doi">10.1038/s41419-020-2275-9</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Review Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>Autophagy in metabolic syndrome: breaking the wheel by targeting the renin–angiotensin system</article-title>
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<contrib contrib-type="author"><name><surname>Rasha</surname>
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<aff id="Aff1"><label>1</label>
<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</aff>
<aff id="Aff2"><label>2</label>
<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</aff>
<aff id="Aff3"><label>3</label>
<institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2179 3554</institution-id>
<institution-id institution-id-type="GRID">grid.416992.1</institution-id>
<institution>Department of Cell Biology and Biochemistry,</institution>
<institution>Texas Tech University Health Sciences Center,</institution>
</institution-wrap>
Lubbock, TX USA</aff>
<aff id="Aff4"><label>4</label>
<institution-wrap><institution-id institution-id-type="ISNI">0000 0000 9816 8637</institution-id>
<institution-id institution-id-type="GRID">grid.11139.3b</institution-id>
<institution>Department of Physiology, Faculty of Medicine,</institution>
<institution>University of Peradeniya,</institution>
</institution-wrap>
Peradeniya, Sri Lanka</aff>
<aff id="Aff5"><label>5</label>
<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</aff>
<aff id="Aff6"><label>6</label>
<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</aff>
</contrib-group>
<pub-date pub-type="epub"><day>3</day>
<month>2</month>
<year>2020</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>3</day>
<month>2</month>
<year>2020</year>
</pub-date>
<pub-date pub-type="collection"><month>2</month>
<year>2020</year>
</pub-date>
<volume>11</volume>
<issue>2</issue>
<elocation-id>87</elocation-id>
<history><date date-type="received"><day>28</day>
<month>9</month>
<year>2019</year>
</date>
<date date-type="rev-recd"><day>8</day>
<month>1</month>
<year>2020</year>
</date>
<date date-type="accepted"><day>9</day>
<month>1</month>
<year>2020</year>
</date>
</history>
<permissions><copyright-statement>© The Author(s) 2020</copyright-statement>
<license license-type="OpenAccess"><license-p><bold>Open Access</bold>
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 <ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">http://creativecommons.org/licenses/by/4.0/</ext-link>
.</license-p>
</license>
</permissions>
<abstract id="Abs1"><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. 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.</p>
</abstract>
<kwd-group kwd-group-type="npg-subject"><title>Subject terms</title>
<kwd>Autophagy</kwd>
<kwd>Obesity</kwd>
</kwd-group>
<funding-group><award-group><funding-source><institution>SPRINT (TTU/FAPESP) Award (NMM, JM, LR)</institution>
</funding-source>
</award-group>
</funding-group>
<custom-meta-group><custom-meta><meta-name>issue-copyright-statement</meta-name>
<meta-value>© The Author(s) 2020</meta-value>
</custom-meta>
</custom-meta-group>
</article-meta>
</front>
</pmc>
</record>
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