Guanxin V alleviates ventricular remodeling by promoting transforming growth factor-beta 1-mediated proteasomal degradation of Vimentin

ABSTRACT: More and more studies have demonstrated that proteasomal degradation occurs in the development of various diseases, including ventricular remodeling, which is a cardiac pathological change and seriously makes patient outcomes worse. Our preliminary results showed that Guanxin V, an effecti...

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Main Authors: Ning Gu, Bo Liang
Format: Article
Language:English
Published: Elsevier 2023-11-01
Series:Poultry Science
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S003257912300545X
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author Ning Gu
Bo Liang
author_facet Ning Gu
Bo Liang
author_sort Ning Gu
collection DOAJ
description ABSTRACT: More and more studies have demonstrated that proteasomal degradation occurs in the development of various diseases, including ventricular remodeling, which is a cardiac pathological change and seriously makes patient outcomes worse. Our preliminary results showed that Guanxin V, an effective and safe complementary and alternative medicine for ventricular remodeling, reverses ventricular hypertrophy by transforming growth factor-beta 1 (TGF-β1), but the specific mechanism needs to be explored. The left anterior descending coronary artery was ligated to build a ventricular remodeling model. Cardiac function and histopathology were measured. Fibrosis-related indicators were detected. Moreover, cardiomyocytes were exposed to hydrogen peroxide to construct an in vitro model of ventricular remodeling. The stability of the Vimentin protein was assessed with cycloheximide and MG132. Endogenous and exogenous TGF-β1-Vimentin interactions were detected by co-immunoprecipitation. Guanxin V significantly eased heart function and improved fibrosis in ventricular remodeling. Mechanistically, Guanxin V promoted TGF-β1-mediated proteasomal degradation of Vimentin and reduced the TGF-β1-Vimentin interaction. Here, we reported a completely new mechanism, Guanxin V alleviates ventricular remodeling by promoting and targeting TGF-β1-mediated proteasomal degradation of Vimentin, which provides a new target for the management of ventricular remodeling and lays the foundation for the further clinical promotion of Guanxin V.
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spelling doaj.art-be90ba5b804f4f4085208dab642d21572023-10-14T04:43:51ZengElsevierPoultry Science0032-57912023-11-0110211103026Guanxin V alleviates ventricular remodeling by promoting transforming growth factor-beta 1-mediated proteasomal degradation of VimentinNing Gu0Bo Liang1Nanjing Hospital of Chinese Medicine Affiliated to Nanjing University of Chinese Medicine, Nanjing 210022, ChinaDepartment of Nephrology, The Key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Chongqing Clinical Research Center of Kidney and Urology Diseases, Xinqiao Hospital, Army Medical University (Third Military Medical University), Chongqing 400037, China; Corresponding author:ABSTRACT: More and more studies have demonstrated that proteasomal degradation occurs in the development of various diseases, including ventricular remodeling, which is a cardiac pathological change and seriously makes patient outcomes worse. Our preliminary results showed that Guanxin V, an effective and safe complementary and alternative medicine for ventricular remodeling, reverses ventricular hypertrophy by transforming growth factor-beta 1 (TGF-β1), but the specific mechanism needs to be explored. The left anterior descending coronary artery was ligated to build a ventricular remodeling model. Cardiac function and histopathology were measured. Fibrosis-related indicators were detected. Moreover, cardiomyocytes were exposed to hydrogen peroxide to construct an in vitro model of ventricular remodeling. The stability of the Vimentin protein was assessed with cycloheximide and MG132. Endogenous and exogenous TGF-β1-Vimentin interactions were detected by co-immunoprecipitation. Guanxin V significantly eased heart function and improved fibrosis in ventricular remodeling. Mechanistically, Guanxin V promoted TGF-β1-mediated proteasomal degradation of Vimentin and reduced the TGF-β1-Vimentin interaction. Here, we reported a completely new mechanism, Guanxin V alleviates ventricular remodeling by promoting and targeting TGF-β1-mediated proteasomal degradation of Vimentin, which provides a new target for the management of ventricular remodeling and lays the foundation for the further clinical promotion of Guanxin V.http://www.sciencedirect.com/science/article/pii/S003257912300545XGuanxin VTGF-β1Vimentinproteasomal degradationventricular remodeling
spellingShingle Ning Gu
Bo Liang
Guanxin V alleviates ventricular remodeling by promoting transforming growth factor-beta 1-mediated proteasomal degradation of Vimentin
Poultry Science
Guanxin V
TGF-β1
Vimentin
proteasomal degradation
ventricular remodeling
title Guanxin V alleviates ventricular remodeling by promoting transforming growth factor-beta 1-mediated proteasomal degradation of Vimentin
title_full Guanxin V alleviates ventricular remodeling by promoting transforming growth factor-beta 1-mediated proteasomal degradation of Vimentin
title_fullStr Guanxin V alleviates ventricular remodeling by promoting transforming growth factor-beta 1-mediated proteasomal degradation of Vimentin
title_full_unstemmed Guanxin V alleviates ventricular remodeling by promoting transforming growth factor-beta 1-mediated proteasomal degradation of Vimentin
title_short Guanxin V alleviates ventricular remodeling by promoting transforming growth factor-beta 1-mediated proteasomal degradation of Vimentin
title_sort guanxin v alleviates ventricular remodeling by promoting transforming growth factor beta 1 mediated proteasomal degradation of vimentin
topic Guanxin V
TGF-β1
Vimentin
proteasomal degradation
ventricular remodeling
url http://www.sciencedirect.com/science/article/pii/S003257912300545X
work_keys_str_mv AT ninggu guanxinvalleviatesventricularremodelingbypromotingtransforminggrowthfactorbeta1mediatedproteasomaldegradationofvimentin
AT boliang guanxinvalleviatesventricularremodelingbypromotingtransforminggrowthfactorbeta1mediatedproteasomaldegradationofvimentin