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Deficiency of GDF-11 Accelerates TAC-Induced Heart Failure by Impairing Cardiac Angiogenesis
The role of growth differentiation factor (GDF)-11 in cardiac diseases has not been fully determined. Our study revealed that GDF-11 is not essential for myocardial development and physiological growth, whereas its absence exacerbates heart failure under pressure overload condition via impairing the...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10322730/ https://www.ncbi.nlm.nih.gov/pubmed/37426531 http://dx.doi.org/10.1016/j.jacbts.2022.11.004 |
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author | Zhu, Jinyun Zhang, Ning Zhao, Yun Liu, Qi Wang, Yingchao Chen, Mingyao Ma, Qunchao Dong, Aiqiang Wang, Yaping Yu, Hong |
author_facet | Zhu, Jinyun Zhang, Ning Zhao, Yun Liu, Qi Wang, Yingchao Chen, Mingyao Ma, Qunchao Dong, Aiqiang Wang, Yaping Yu, Hong |
author_sort | Zhu, Jinyun |
collection | PubMed |
description | The role of growth differentiation factor (GDF)-11 in cardiac diseases has not been fully determined. Our study revealed that GDF-11 is not essential for myocardial development and physiological growth, whereas its absence exacerbates heart failure under pressure overload condition via impairing the responsive angiogenesis. GDF-11 induced VEGF expression in CMs by activating the Akt/mTOR pathway. The effect of endogenous GDF-11 on the heart belongs to local self-regulation of myocardial tissue, rather than a way of systemic regulation. |
format | Online Article Text |
id | pubmed-10322730 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-103227302023-07-07 Deficiency of GDF-11 Accelerates TAC-Induced Heart Failure by Impairing Cardiac Angiogenesis Zhu, Jinyun Zhang, Ning Zhao, Yun Liu, Qi Wang, Yingchao Chen, Mingyao Ma, Qunchao Dong, Aiqiang Wang, Yaping Yu, Hong JACC Basic Transl Sci Original Research - Preclinical The role of growth differentiation factor (GDF)-11 in cardiac diseases has not been fully determined. Our study revealed that GDF-11 is not essential for myocardial development and physiological growth, whereas its absence exacerbates heart failure under pressure overload condition via impairing the responsive angiogenesis. GDF-11 induced VEGF expression in CMs by activating the Akt/mTOR pathway. The effect of endogenous GDF-11 on the heart belongs to local self-regulation of myocardial tissue, rather than a way of systemic regulation. Elsevier 2023-02-22 /pmc/articles/PMC10322730/ /pubmed/37426531 http://dx.doi.org/10.1016/j.jacbts.2022.11.004 Text en © 2023 Published by Elsevier on behalf of the American College of Cardiology Foundation. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Original Research - Preclinical Zhu, Jinyun Zhang, Ning Zhao, Yun Liu, Qi Wang, Yingchao Chen, Mingyao Ma, Qunchao Dong, Aiqiang Wang, Yaping Yu, Hong Deficiency of GDF-11 Accelerates TAC-Induced Heart Failure by Impairing Cardiac Angiogenesis |
title | Deficiency of GDF-11 Accelerates TAC-Induced Heart Failure by Impairing Cardiac Angiogenesis |
title_full | Deficiency of GDF-11 Accelerates TAC-Induced Heart Failure by Impairing Cardiac Angiogenesis |
title_fullStr | Deficiency of GDF-11 Accelerates TAC-Induced Heart Failure by Impairing Cardiac Angiogenesis |
title_full_unstemmed | Deficiency of GDF-11 Accelerates TAC-Induced Heart Failure by Impairing Cardiac Angiogenesis |
title_short | Deficiency of GDF-11 Accelerates TAC-Induced Heart Failure by Impairing Cardiac Angiogenesis |
title_sort | deficiency of gdf-11 accelerates tac-induced heart failure by impairing cardiac angiogenesis |
topic | Original Research - Preclinical |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10322730/ https://www.ncbi.nlm.nih.gov/pubmed/37426531 http://dx.doi.org/10.1016/j.jacbts.2022.11.004 |
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