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Remodeling and Fibrosis of the Cardiac Muscle in the Course of Obesity—Pathogenesis and Involvement of the Extracellular Matrix

Obesity is a growing epidemiological problem, as two-thirds of the adult population are carrying excess weight. It is a risk factor for the development of cardiovascular diseases (hypertension, ischemic heart disease, myocardial infarct, and atrial fibrillation). It has also been shown that chronic...

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Autores principales: Kruszewska, Jagoda, Cudnoch-Jedrzejewska, Agnieszka, Czarzasta, Katarzyna
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9032681/
https://www.ncbi.nlm.nih.gov/pubmed/35457013
http://dx.doi.org/10.3390/ijms23084195
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author Kruszewska, Jagoda
Cudnoch-Jedrzejewska, Agnieszka
Czarzasta, Katarzyna
author_facet Kruszewska, Jagoda
Cudnoch-Jedrzejewska, Agnieszka
Czarzasta, Katarzyna
author_sort Kruszewska, Jagoda
collection PubMed
description Obesity is a growing epidemiological problem, as two-thirds of the adult population are carrying excess weight. It is a risk factor for the development of cardiovascular diseases (hypertension, ischemic heart disease, myocardial infarct, and atrial fibrillation). It has also been shown that chronic obesity in people may be a cause for the development of heart failure with preserved ejection fraction (HFpEF), whose components include cellular hypertrophy, left ventricular diastolic dysfunction, and increased extracellular collagen deposition. Several animal models with induced obesity, via the administration of a high-fat diet, also developed increased heart fibrosis as a result of extracellular collagen accumulation. Excessive collagen deposition in the extracellular matrix (ECM) in the course of obesity may increase the stiffness of the myocardium and thereby deteriorate the heart diastolic function and facilitate the occurrence of HFpEF. In this review, we include a rationale for that process, including a discussion about possible putative factors (such as increased renin–angiotensin–aldosterone activity, sympathetic overdrive, hemodynamic alterations, hypoadiponectinemia, hyperleptinemia, and concomitant heart diseases). To address the topic clearly, we include a description of the fundamentals of ECM turnover, as well as a summary of studies assessing collagen deposition in obese individuals.
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spelling pubmed-90326812022-04-23 Remodeling and Fibrosis of the Cardiac Muscle in the Course of Obesity—Pathogenesis and Involvement of the Extracellular Matrix Kruszewska, Jagoda Cudnoch-Jedrzejewska, Agnieszka Czarzasta, Katarzyna Int J Mol Sci Review Obesity is a growing epidemiological problem, as two-thirds of the adult population are carrying excess weight. It is a risk factor for the development of cardiovascular diseases (hypertension, ischemic heart disease, myocardial infarct, and atrial fibrillation). It has also been shown that chronic obesity in people may be a cause for the development of heart failure with preserved ejection fraction (HFpEF), whose components include cellular hypertrophy, left ventricular diastolic dysfunction, and increased extracellular collagen deposition. Several animal models with induced obesity, via the administration of a high-fat diet, also developed increased heart fibrosis as a result of extracellular collagen accumulation. Excessive collagen deposition in the extracellular matrix (ECM) in the course of obesity may increase the stiffness of the myocardium and thereby deteriorate the heart diastolic function and facilitate the occurrence of HFpEF. In this review, we include a rationale for that process, including a discussion about possible putative factors (such as increased renin–angiotensin–aldosterone activity, sympathetic overdrive, hemodynamic alterations, hypoadiponectinemia, hyperleptinemia, and concomitant heart diseases). To address the topic clearly, we include a description of the fundamentals of ECM turnover, as well as a summary of studies assessing collagen deposition in obese individuals. MDPI 2022-04-11 /pmc/articles/PMC9032681/ /pubmed/35457013 http://dx.doi.org/10.3390/ijms23084195 Text en © 2022 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 Review
Kruszewska, Jagoda
Cudnoch-Jedrzejewska, Agnieszka
Czarzasta, Katarzyna
Remodeling and Fibrosis of the Cardiac Muscle in the Course of Obesity—Pathogenesis and Involvement of the Extracellular Matrix
title Remodeling and Fibrosis of the Cardiac Muscle in the Course of Obesity—Pathogenesis and Involvement of the Extracellular Matrix
title_full Remodeling and Fibrosis of the Cardiac Muscle in the Course of Obesity—Pathogenesis and Involvement of the Extracellular Matrix
title_fullStr Remodeling and Fibrosis of the Cardiac Muscle in the Course of Obesity—Pathogenesis and Involvement of the Extracellular Matrix
title_full_unstemmed Remodeling and Fibrosis of the Cardiac Muscle in the Course of Obesity—Pathogenesis and Involvement of the Extracellular Matrix
title_short Remodeling and Fibrosis of the Cardiac Muscle in the Course of Obesity—Pathogenesis and Involvement of the Extracellular Matrix
title_sort remodeling and fibrosis of the cardiac muscle in the course of obesity—pathogenesis and involvement of the extracellular matrix
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9032681/
https://www.ncbi.nlm.nih.gov/pubmed/35457013
http://dx.doi.org/10.3390/ijms23084195
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