Placental extract suppresses cardiac hypertrophy and fibrosis in an angiotensin II-induced cachexia model in mice

Cachexia is an intractable metabolic disorder that causes extreme weight loss. It is a symptom of many chronic diseases, including cancer, liver failure, congestive heart failure and chronic kidney disease, and there is as yet no effective treatment. While the mechanisms underlying cachexia are comp...

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Main Authors: Akihiro Yamauchi, Akiko Kamiyoshi, Takayuki Sakurai, Hiroyuki Miyazaki, Eiichi Hirano, Hong Seok Lim, Taiichi Kaku, Takayuki Shindo
Format: Article
Language:English
Published: Elsevier 2019-10-01
Series:Heliyon
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S2405844019363157
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author Akihiro Yamauchi
Akiko Kamiyoshi
Takayuki Sakurai
Hiroyuki Miyazaki
Eiichi Hirano
Hong Seok Lim
Taiichi Kaku
Takayuki Shindo
author_facet Akihiro Yamauchi
Akiko Kamiyoshi
Takayuki Sakurai
Hiroyuki Miyazaki
Eiichi Hirano
Hong Seok Lim
Taiichi Kaku
Takayuki Shindo
author_sort Akihiro Yamauchi
collection DOAJ
description Cachexia is an intractable metabolic disorder that causes extreme weight loss. It is a symptom of many chronic diseases, including cancer, liver failure, congestive heart failure and chronic kidney disease, and there is as yet no effective treatment. While the mechanisms underlying cachexia are complex, it is often accompanied by elevated angiotensin II (Ang II). Human placental extract (HPE) is a source of numerous biologically active molecules and has been used clinically to treat chronic hepatitis, liver cirrhosis and other chronic diseases. Here, we investigated the effects of HPE in an Ang II-induced cachexia model in mice. HPE treatment preserved both fat mass and lean body mass and suppressed weight loss in the cachexia model, though food intake was unaffected. Ang II infusion also caused cardiac hypertrophy and fibrosis. HPE suppressed these effects as well as Ang II-induced cardiac expression of genes related to heart failure and cardiac remodeling. HPE also reversed Ang II-induced downregulation of mitochondria-related molecules and suppressed cardiac inflammation and oxidative stress. HPE administration may thus be an effective approach to the treatment of cachexia, cardiac hypertrophy and fibrosis.
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spelling doaj.art-dd3e70cfce9944edbf529d477d40f4182022-12-21T22:46:21ZengElsevierHeliyon2405-84402019-10-01510e02655Placental extract suppresses cardiac hypertrophy and fibrosis in an angiotensin II-induced cachexia model in miceAkihiro Yamauchi0Akiko Kamiyoshi1Takayuki Sakurai2Hiroyuki Miyazaki3Eiichi Hirano4Hong Seok Lim5Taiichi Kaku6Takayuki Shindo7Department of Cardiovascular Research, Shinshu University Graduate School of Medicine, Matsumoto, Japan; Japan Bio Products Co., Ltd., Tokyo, JapanDepartment of Cardiovascular Research, Shinshu University Graduate School of Medicine, Matsumoto, JapanDepartment of Cardiovascular Research, Shinshu University Graduate School of Medicine, Matsumoto, JapanJapan Bio Products Co., Ltd., Tokyo, JapanJapan Bio Products Co., Ltd., Tokyo, JapanJapan Bio Products Co., Ltd., Tokyo, JapanJapan Bio Products Co., Ltd., Tokyo, JapanDepartment of Cardiovascular Research, Shinshu University Graduate School of Medicine, Matsumoto, Japan; Corresponding author.Cachexia is an intractable metabolic disorder that causes extreme weight loss. It is a symptom of many chronic diseases, including cancer, liver failure, congestive heart failure and chronic kidney disease, and there is as yet no effective treatment. While the mechanisms underlying cachexia are complex, it is often accompanied by elevated angiotensin II (Ang II). Human placental extract (HPE) is a source of numerous biologically active molecules and has been used clinically to treat chronic hepatitis, liver cirrhosis and other chronic diseases. Here, we investigated the effects of HPE in an Ang II-induced cachexia model in mice. HPE treatment preserved both fat mass and lean body mass and suppressed weight loss in the cachexia model, though food intake was unaffected. Ang II infusion also caused cardiac hypertrophy and fibrosis. HPE suppressed these effects as well as Ang II-induced cardiac expression of genes related to heart failure and cardiac remodeling. HPE also reversed Ang II-induced downregulation of mitochondria-related molecules and suppressed cardiac inflammation and oxidative stress. HPE administration may thus be an effective approach to the treatment of cachexia, cardiac hypertrophy and fibrosis.http://www.sciencedirect.com/science/article/pii/S2405844019363157BiochemistryCardiac hypertrophyHuman placenta extractCardiac fibrosisAngiotensin IICachexia
spellingShingle Akihiro Yamauchi
Akiko Kamiyoshi
Takayuki Sakurai
Hiroyuki Miyazaki
Eiichi Hirano
Hong Seok Lim
Taiichi Kaku
Takayuki Shindo
Placental extract suppresses cardiac hypertrophy and fibrosis in an angiotensin II-induced cachexia model in mice
Heliyon
Biochemistry
Cardiac hypertrophy
Human placenta extract
Cardiac fibrosis
Angiotensin II
Cachexia
title Placental extract suppresses cardiac hypertrophy and fibrosis in an angiotensin II-induced cachexia model in mice
title_full Placental extract suppresses cardiac hypertrophy and fibrosis in an angiotensin II-induced cachexia model in mice
title_fullStr Placental extract suppresses cardiac hypertrophy and fibrosis in an angiotensin II-induced cachexia model in mice
title_full_unstemmed Placental extract suppresses cardiac hypertrophy and fibrosis in an angiotensin II-induced cachexia model in mice
title_short Placental extract suppresses cardiac hypertrophy and fibrosis in an angiotensin II-induced cachexia model in mice
title_sort placental extract suppresses cardiac hypertrophy and fibrosis in an angiotensin ii induced cachexia model in mice
topic Biochemistry
Cardiac hypertrophy
Human placenta extract
Cardiac fibrosis
Angiotensin II
Cachexia
url http://www.sciencedirect.com/science/article/pii/S2405844019363157
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