Autophagy in metabolic syndrome: breaking the wheel by targeting the renin–angiotensin system
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 ev...
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| Published in | Cell death & disease Vol. 11; no. 2; p. 87 |
|---|---|
| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
03.02.2020
Springer Nature B.V |
| Subjects | |
| Online Access | Get full text |
| ISSN | 2041-4889 2041-4889 |
| DOI | 10.1038/s41419-020-2275-9 |
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| 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. |
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| AbstractList | 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.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. 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. |
| ArticleNumber | 87 |
| Author | Moustaid-Moussa, Naima Kalupahana, Nishan S. Sunahara, Karen K. S. Wang, Shu Martins, Joilson O. Menikdiwela, Kalhara R. Rasha, Fahmida Dufour, Jannette M. Ramalingam, Latha |
| Author_xml | – sequence: 1 givenname: Kalhara R. surname: Menikdiwela fullname: Menikdiwela, Kalhara R. organization: Department of Nutritional Sciences, Texas Tech University, Obesity Research Institute, Texas Tech University – sequence: 2 givenname: Latha surname: Ramalingam fullname: Ramalingam, Latha organization: Department of Nutritional Sciences, Texas Tech University, Obesity Research Institute, Texas Tech University – sequence: 3 givenname: Fahmida surname: Rasha fullname: Rasha, Fahmida organization: Department of Nutritional Sciences, Texas Tech University, Obesity Research Institute, Texas Tech University – sequence: 4 givenname: Shu orcidid: 0000-0001-8078-9942 surname: Wang fullname: Wang, Shu organization: Department of Nutritional Sciences, Texas Tech University, Obesity Research Institute, Texas Tech University – sequence: 5 givenname: Jannette M. surname: Dufour fullname: Dufour, Jannette M. organization: Obesity Research Institute, Texas Tech University, Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center – sequence: 6 givenname: Nishan S. surname: Kalupahana fullname: Kalupahana, Nishan S. organization: Department of Nutritional Sciences, Texas Tech University, Obesity Research Institute, Texas Tech University, Department of Physiology, Faculty of Medicine, University of Peradeniya – sequence: 7 givenname: Karen K. S. surname: Sunahara fullname: Sunahara, Karen K. S. organization: Department of Experimental Physiopatholgy, Medical School University of São Paulo – sequence: 8 givenname: Joilson O. orcidid: 0000-0003-2630-7038 surname: Martins fullname: Martins, Joilson O. organization: Laboratory of Immunoendocrinology, Department of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences of University Sao Paulo (FCF/USP) – sequence: 9 givenname: Naima orcidid: 0000-0002-7508-8030 surname: Moustaid-Moussa fullname: Moustaid-Moussa, Naima email: naima.moustaid-moussa@ttu.edu organization: Department of Nutritional Sciences, Texas Tech University, Obesity Research Institute, Texas Tech University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32015340$$D View this record in MEDLINE/PubMed |
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| Title | Autophagy in metabolic syndrome: breaking the wheel by targeting the renin–angiotensin system |
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