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Extracellular Matrix in Heart Disease 2.0
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Extracellular Matrix in Heart Disease 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 13768

Special Issue Editor

Dr. Muneyoshi Okada

E-Mail Website
Guest Editor
Laboratory of Veterinary Pharmacology, School of Veterinary Medicine, Kitasato University, Higashi 23 bancho 35–1, Towada, Aomori 034–8628, Japan
Interests: cardiovascular pharmacology; cardiovascular disease; myocardial infarction; cardiac hypertrophy; arrhythmia; heart failure; pulmonary arterial hypertension; fibrosis; extracellular matrix; cardiac fibroblast; cardiomyocyte; matricryptin/matrikine; matricellular protein; matrix metalloproteinase; cardiac electrophysiology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Components of the extracellular matrix (ECM), such as collagen, fibronectin, laminin, and proteoglycan, maintain cardiac structure and function by forming a complicated three-dimensional network. Cell–ECM interaction is also important for regulating the functions of cardiomyocytes and non-cardiomyocytes. An imbalance between the production and degradation of the ECM during the development and progression of heart disease is associated with pathological cardiac remodeling, including hypertrophy and fibrosis. Recently, it has been reported that matricellular proteins, a family of non-structural ECM proteins, and matricryptins/matrikines, bioactive fragments of ECM proteins, are involved in cardiac remodeling. In this Special Issue, we expect to gather novel knowledge that will lead to the discovery of drugs targeting the ECM and its fragments for heart disease.

Dr. Muneyoshi Okada
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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Keywords

  • extracellular matrix
  • cardiac remodeling
  • fibrosis
  • hypertrophy
  • heart failure
  • fibroblast
  • cardiomyocyte
  • matricryptin/matrikine
  • matricellular protein
  • matrix metalloproteinase

Related Special Issue

Published Papers (5 papers)

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Research

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16 pages, 2379 KiB  
Article
Decreased Substrate Stiffness Promotes a Hypofibrotic Phenotype in Cardiac Fibroblasts
by Rachel C. Childers, Pamela A. Lucchesi and Keith J. Gooch
Int. J. Mol. Sci. 2021, 22(12), 6231; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22126231 - 09 Jun 2021
Cited by 9 | Viewed by 2163
Abstract
A hypofibrotic phenotype has been observed in cardiac fibroblasts (CFs) isolated from a volume overload heart failure model, aortocaval fistula (ACF). This paradoxical phenotype results in decreased ECM synthesis despite increased TGF-β presence. Since ACF results in decreased tissue stiffness relative to control [...] Read more.
A hypofibrotic phenotype has been observed in cardiac fibroblasts (CFs) isolated from a volume overload heart failure model, aortocaval fistula (ACF). This paradoxical phenotype results in decreased ECM synthesis despite increased TGF-β presence. Since ACF results in decreased tissue stiffness relative to control (sham) hearts, this study investigates whether the effects of substrate stiffness could account for the observed hypofibrotic phenotype in CFs isolated from ACF. CFs isolated from ACF and sham hearts were plated on polyacrylamide gels of a range of stiffness (2 kPa to 50 kPa). Markers related to cytoskeletal and fibrotic proteins were measured. Aspects of the hypofibrotic phenotype observed in ACF CFs were recapitulated by sham CFs on soft substrates. For instance, sham CFs on the softest gels compared to ACF CFs on the stiffest gels results in similar CTGF (0.80 vs. 0.76) and transgelin (0.44 vs. 0.57) mRNA expression. The changes due to stiffness may be explained by the observed decreased nuclear translocation of transcriptional regulators, MRTF-A and YAP. ACF CFs appear to have a mechanical memory of a softer environment, supported by a hypofibrotic phenotype overall compared to sham with less YAP detected in the nucleus, and less CTGF and transgelin on all stiffnesses. Full article
(This article belongs to the Special Issue Extracellular Matrix in Heart Disease 2.0)
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15 pages, 2994 KiB  
Article
Matrix Metalloproteinases and Their Role in Mechanisms Underlying Effects of Quercetin on Heart Function in Aged Zucker Diabetic Fatty Rats
by Barbora Boťanská, Monika Barteková, Kristína Ferenczyová, Mária Fogarassyová, Lucia Kindernay and Miroslav Barančík
Int. J. Mol. Sci. 2021, 22(9), 4457; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094457 - 24 Apr 2021
Cited by 7 | Viewed by 1931
Abstract
Several mechanisms may contribute to cardiovascular pathology associated with diabetes, including dysregulation of matrix metalloproteinases (MMPs). Quercetin (QCT) is a substance with preventive effects in treatment of cardiovascular diseases and diabetes. The aim of the present study was to explore effects of chronic [...] Read more.
Several mechanisms may contribute to cardiovascular pathology associated with diabetes, including dysregulation of matrix metalloproteinases (MMPs). Quercetin (QCT) is a substance with preventive effects in treatment of cardiovascular diseases and diabetes. The aim of the present study was to explore effects of chronic QCT administration on changes in heart function in aged lean and obese Zucker Diabetic Fatty (ZDF) rats and that in association with MMPs. Signaling underlying effects of diabetes and QCT were also investigated. In the study, we used one-year-old lean and obese ZDF rats treated for 6 weeks with QCT. Results showed that obesity worsened heart function and this was associated with MMP-2 upregulation, MMP-28 downregulation, and inhibition of superoxide dismutases (SODs). Treatment with QCT did not modulate diabetes-induced changes in heart function and MMPs. However, QCT activated Akt kinase and reversed effects of diabetes on SODs inhibition. In conclusion, worsened heart function due to obesity involved changes in MMP-2 and MMP-28 and attenuation of antioxidant defense by SOD. QCT did not have positive effects on improvement of heart function or modulation of MMPs. Nevertheless, its application mediated activation of adaptive responses against oxidative stress through Akt kinase and prevention of diabetes-induced negative effects on antioxidant defense by SODs. Full article
(This article belongs to the Special Issue Extracellular Matrix in Heart Disease 2.0)
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10 pages, 2627 KiB  
Article
Preventive Effect of Canstatin against Ventricular Arrhythmia Induced by Ischemia/Reperfusion Injury: A Pilot Study
by Akira Sugiyama, Yurie Shimizu, Muneyoshi Okada, Kosuke Otani and Hideyuki Yamawaki
Int. J. Mol. Sci. 2021, 22(3), 1004; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22031004 - 20 Jan 2021
Cited by 7 | Viewed by 2003
Abstract
Ventricular arrhythmia induced by ischemia/reperfusion (I/R) injury is a clinical problem in reperfusion therapies for acute myocardial infarction. Ca2+ overload through reactive oxygen species (ROS) production is a major cause for I/R-induced arrhythmia. We previously demonstrated that canstatin, a C-terminal fragment of [...] Read more.
Ventricular arrhythmia induced by ischemia/reperfusion (I/R) injury is a clinical problem in reperfusion therapies for acute myocardial infarction. Ca2+ overload through reactive oxygen species (ROS) production is a major cause for I/R-induced arrhythmia. We previously demonstrated that canstatin, a C-terminal fragment of type IV collagen α2 chain, regulated Ca2+ handling in rat heart. In this study, we aimed to clarify the effects of canstatin on I/R-induced ventricular arrhythmia in rats. Male Wistar rats were subjected to I/R injury by ligating the left anterior descending artery followed by reperfusion. Ventricular arrhythmia (ventricular tachycardia and ventricular fibrillation) was recorded by electrocardiogram. Nicotinamide adenine dinucleotide phosphate oxidase (NOX) activity and ROS production in neonatal rat cardiomyocytes (NRCMs) stimulated with oxygen glucose deprivation/reperfusion (OGD/R) were measured by lucigenin assay and 2′,7′-dichlorodihydrofluorescein diacetate staining, respectively. The H2O2-induced intracellular Ca2+ ([Ca2+]i) rise in NRCMs was measured by a fluorescent Ca2+ indicator. Canstatin (20 µg/kg) inhibited I/R-induced ventricular arrhythmia in rats. Canstatin (250 ng/mL) inhibited OGD/R-induced NOX activation and ROS production and suppressed the H2O2-induced [Ca2+]i rise in NRCMs. We for the first time demonstrated that canstatin exerts a preventive effect against I/R-induced ventricular arrhythmia, perhaps in part through the suppression of ROS production and the subsequent [Ca2+]i rise. Full article
(This article belongs to the Special Issue Extracellular Matrix in Heart Disease 2.0)
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15 pages, 4682 KiB  
Article
The Histamine 3 Receptor Is Expressed in the Heart and Its Activation Opposes Adverse Cardiac Remodeling in the Angiotensin II Mouse Model
by Samuel L. McCaffrey, Grace Lim, Martyn Bullock, Ainsley O. Kasparian, Roderick Clifton-Bligh, William B. Campbell, Alexander Widiapradja and Scott P. Levick
Int. J. Mol. Sci. 2020, 21(24), 9757; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21249757 - 21 Dec 2020
Cited by 6 | Viewed by 2211
Abstract
Histamine is a basic amine stored in mast cells, with its release capable of activating one of four histamine receptors. The histamine 3 receptor (H3R) is known to be cardioprotective during acute ischemia by acting to limit norepinephrine release. However, a [...] Read more.
Histamine is a basic amine stored in mast cells, with its release capable of activating one of four histamine receptors. The histamine 3 receptor (H3R) is known to be cardioprotective during acute ischemia by acting to limit norepinephrine release. However, a recent study reported that myofibroblasts isolated from the infarct zone of rat hearts responded to H3R activation by up-regulating collagen production. Thus, it is necessary to clarify the potential role of the H3R in relation to fibrosis in the heart. We identified that the mouse left ventricle (LV) expresses the H3R. Isolation of mouse cardiac fibroblasts determined that while angiotensin II (Ang II) increased levels of the H3R, these cells did not produce excess collagen in response to H3R activation. Using the Ang II mouse model of adverse cardiac remodeling, we found that while H3R blockade had little effect on cardiac fibrosis, activation of the H3R reduced cardiac fibrosis and macrophage infiltration. These findings suggest that when activated, the H3R is anti-inflammatory and anti-fibrotic in the mouse heart and may be a promising target for protecting against cardiac fibrosis. Full article
(This article belongs to the Special Issue Extracellular Matrix in Heart Disease 2.0)
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Review

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21 pages, 1113 KiB  
Review
Extracellular Matrix in Calcific Aortic Valve Disease: Architecture, Dynamic and Perspectives
by Anna Di Vito, Annalidia Donato, Ivan Presta, Teresa Mancuso, Francesco Saverio Brunetti, Pasquale Mastroroberto, Andrea Amorosi, Natalia Malara and Giuseppe Donato
Int. J. Mol. Sci. 2021, 22(2), 913; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22020913 - 18 Jan 2021
Cited by 44 | Viewed by 4661
Abstract
Calcific Aortic Valve Disease (CAVD) is the most common valvular heart disease in developed countries and in the ageing population. It is strongly correlated to median age, affecting up to 13% of the population over the age of 65. Pathophysiological analysis indicates CAVD [...] Read more.
Calcific Aortic Valve Disease (CAVD) is the most common valvular heart disease in developed countries and in the ageing population. It is strongly correlated to median age, affecting up to 13% of the population over the age of 65. Pathophysiological analysis indicates CAVD as a result of an active and degenerative disease, starting with sclerosis and chronic inflammation and then leaflet calcification, which ultimately can account for aortic stenosis. Although CAVD has been firstly recognized as a passive event mostly resulting from a degenerative aging process, much evidences suggests that calcification arises from different active processes, involving both aortic valve-resident cells (valve endothelial cells, valve interstitial cells, mesenchymal stem cells, innate immunity cells) and circulating cells (circulating mesenchymal cells, immunity cells). Moreover, a role for the cell-derived “matrix vesicles” and extracellular matrix (ECM) components has also been recognized. The aim of this work is to review the cellular and molecular alterations occurring in aortic valve during CAVD pathogenesis, focusing on the role of ECM in the natural course of the disease. Full article
(This article belongs to the Special Issue Extracellular Matrix in Heart Disease 2.0)
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