Abstinence Restores Cardiac Function in Mice with Established Alcohol-Induced Cardiomyopathy
Alcohol-induced cardiomyopathy (ACM) has a poor prognosis with up to a 50% chance of death within four years of diagnosis. There are limited studies investigating the potential of abstinence for promoting repair after alcohol-induced cardiac damage, particularly in a controlled preclinical study des...
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MDPI AG
2023-12-01
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Online Access: | https://www.mdpi.com/2073-4409/12/24/2783 |
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author | Joshua M. Edavettal Nicholas R. Harris Sarah E. Cohen Janos Paloczi Bysani Chandrasekar Jason D. Gardner |
author_facet | Joshua M. Edavettal Nicholas R. Harris Sarah E. Cohen Janos Paloczi Bysani Chandrasekar Jason D. Gardner |
author_sort | Joshua M. Edavettal |
collection | DOAJ |
description | Alcohol-induced cardiomyopathy (ACM) has a poor prognosis with up to a 50% chance of death within four years of diagnosis. There are limited studies investigating the potential of abstinence for promoting repair after alcohol-induced cardiac damage, particularly in a controlled preclinical study design. Here, we developed an exposure protocol that led to significant decreases in cardiac function in C57BL6/J mice within 30 days; dP/dt max decreased in the mice fed alcohol for 30 days (8054 ± 664.5 mmHg/s compared to control mice: 11,188 ± 724.2 mmHg/s, <i>p</i> < 0.01), and the dP/dt min decreased, as well (−7711 ± 561 mmHg/s compared to control mice: −10,147 ± 448.2 mmHg/s, <i>p</i> < 0.01). Quantitative PCR was used to investigate inflammatory and fibrotic biomarkers, while histology was used to depict overt changes in cardiac fibrosis. We observed a complete recovery of function after abstinence (dP/dt max increased from 8054 ± 664 mmHg/s at 30 days to 11,967 ± 449 mmHg/s after abstinence, <i>p</i> < 0.01); further, both inflammatory and fibrotic biomarkers decreased after abstinence. These results lay the groundwork for future investigation of the molecular mechanisms underlying recovery from alcohol-induced damage in the heart. |
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issn | 2073-4409 |
language | English |
last_indexed | 2024-03-08T20:54:32Z |
publishDate | 2023-12-01 |
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spelling | doaj.art-39d2519b1b4f46119b52eff95ff2e83f2023-12-22T13:59:34ZengMDPI AGCells2073-44092023-12-011224278310.3390/cells12242783Abstinence Restores Cardiac Function in Mice with Established Alcohol-Induced CardiomyopathyJoshua M. Edavettal0Nicholas R. Harris1Sarah E. Cohen2Janos Paloczi3Bysani Chandrasekar4Jason D. Gardner5Department of Physiology, LSU Health Sciences Center—New Orleans, New Orleans, LA 70112, USADepartment of Physiology, LSU Health Sciences Center—New Orleans, New Orleans, LA 70112, USADepartment of Physiology, LSU Health Sciences Center—New Orleans, New Orleans, LA 70112, USADepartment of Physiology, LSU Health Sciences Center—New Orleans, New Orleans, LA 70112, USADepartment of Medicine, University of Missouri School of Medicine, Columbia, MO 65212, USADepartment of Physiology, LSU Health Sciences Center—New Orleans, New Orleans, LA 70112, USAAlcohol-induced cardiomyopathy (ACM) has a poor prognosis with up to a 50% chance of death within four years of diagnosis. There are limited studies investigating the potential of abstinence for promoting repair after alcohol-induced cardiac damage, particularly in a controlled preclinical study design. Here, we developed an exposure protocol that led to significant decreases in cardiac function in C57BL6/J mice within 30 days; dP/dt max decreased in the mice fed alcohol for 30 days (8054 ± 664.5 mmHg/s compared to control mice: 11,188 ± 724.2 mmHg/s, <i>p</i> < 0.01), and the dP/dt min decreased, as well (−7711 ± 561 mmHg/s compared to control mice: −10,147 ± 448.2 mmHg/s, <i>p</i> < 0.01). Quantitative PCR was used to investigate inflammatory and fibrotic biomarkers, while histology was used to depict overt changes in cardiac fibrosis. We observed a complete recovery of function after abstinence (dP/dt max increased from 8054 ± 664 mmHg/s at 30 days to 11,967 ± 449 mmHg/s after abstinence, <i>p</i> < 0.01); further, both inflammatory and fibrotic biomarkers decreased after abstinence. These results lay the groundwork for future investigation of the molecular mechanisms underlying recovery from alcohol-induced damage in the heart.https://www.mdpi.com/2073-4409/12/24/2783alcohol-induced cardiomyopathyabstinencereversalcardiac function |
spellingShingle | Joshua M. Edavettal Nicholas R. Harris Sarah E. Cohen Janos Paloczi Bysani Chandrasekar Jason D. Gardner Abstinence Restores Cardiac Function in Mice with Established Alcohol-Induced Cardiomyopathy Cells alcohol-induced cardiomyopathy abstinence reversal cardiac function |
title | Abstinence Restores Cardiac Function in Mice with Established Alcohol-Induced Cardiomyopathy |
title_full | Abstinence Restores Cardiac Function in Mice with Established Alcohol-Induced Cardiomyopathy |
title_fullStr | Abstinence Restores Cardiac Function in Mice with Established Alcohol-Induced Cardiomyopathy |
title_full_unstemmed | Abstinence Restores Cardiac Function in Mice with Established Alcohol-Induced Cardiomyopathy |
title_short | Abstinence Restores Cardiac Function in Mice with Established Alcohol-Induced Cardiomyopathy |
title_sort | abstinence restores cardiac function in mice with established alcohol induced cardiomyopathy |
topic | alcohol-induced cardiomyopathy abstinence reversal cardiac function |
url | https://www.mdpi.com/2073-4409/12/24/2783 |
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