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Tumor Growth Ameliorates Cardiac Dysfunction
Heart failure and cancer are the deadliest diseases worldwide. Murine models for cardiac remodeling and heart failure demonstrate that cardiac dysfunction promotes cancer progression and metastasis spread. Yet, no information is available on whether and how tumor progression affects cardiac remodeli...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10378697/ https://www.ncbi.nlm.nih.gov/pubmed/37508517 http://dx.doi.org/10.3390/cells12141853 |
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author | Awwad, Lama Shofti, Rona Haas, Tali Aronheim, Ami |
author_facet | Awwad, Lama Shofti, Rona Haas, Tali Aronheim, Ami |
author_sort | Awwad, Lama |
collection | PubMed |
description | Heart failure and cancer are the deadliest diseases worldwide. Murine models for cardiac remodeling and heart failure demonstrate that cardiac dysfunction promotes cancer progression and metastasis spread. Yet, no information is available on whether and how tumor progression affects cardiac remodeling. Here, we examined cardiac remodeling following transverse aortic constriction (TAC) in the presence or absence of proliferating cancer cells. We show that tumor-bearing mice, of two different cancer cell lines, display reduced cardiac hypertrophy, lower fibrosis and improved cardiac contractile function following pressure overload induced by TAC surgery. Integrative analysis of qRT-PCR, flow cytometry and immunofluorescence identified tumor-dependent M1-to-M2 polarization in the cardiac macrophage population as a mediator of the beneficial tumor effect on the heart. Importantly, tumor-bearing mice lacking functional macrophages fail to improve cardiac function and display sustained fibrosis. |
format | Online Article Text |
id | pubmed-10378697 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-103786972023-07-29 Tumor Growth Ameliorates Cardiac Dysfunction Awwad, Lama Shofti, Rona Haas, Tali Aronheim, Ami Cells Article Heart failure and cancer are the deadliest diseases worldwide. Murine models for cardiac remodeling and heart failure demonstrate that cardiac dysfunction promotes cancer progression and metastasis spread. Yet, no information is available on whether and how tumor progression affects cardiac remodeling. Here, we examined cardiac remodeling following transverse aortic constriction (TAC) in the presence or absence of proliferating cancer cells. We show that tumor-bearing mice, of two different cancer cell lines, display reduced cardiac hypertrophy, lower fibrosis and improved cardiac contractile function following pressure overload induced by TAC surgery. Integrative analysis of qRT-PCR, flow cytometry and immunofluorescence identified tumor-dependent M1-to-M2 polarization in the cardiac macrophage population as a mediator of the beneficial tumor effect on the heart. Importantly, tumor-bearing mice lacking functional macrophages fail to improve cardiac function and display sustained fibrosis. MDPI 2023-07-14 /pmc/articles/PMC10378697/ /pubmed/37508517 http://dx.doi.org/10.3390/cells12141853 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Awwad, Lama Shofti, Rona Haas, Tali Aronheim, Ami Tumor Growth Ameliorates Cardiac Dysfunction |
title | Tumor Growth Ameliorates Cardiac Dysfunction |
title_full | Tumor Growth Ameliorates Cardiac Dysfunction |
title_fullStr | Tumor Growth Ameliorates Cardiac Dysfunction |
title_full_unstemmed | Tumor Growth Ameliorates Cardiac Dysfunction |
title_short | Tumor Growth Ameliorates Cardiac Dysfunction |
title_sort | tumor growth ameliorates cardiac dysfunction |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10378697/ https://www.ncbi.nlm.nih.gov/pubmed/37508517 http://dx.doi.org/10.3390/cells12141853 |
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