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Role of Mitochondrial Dysfunction in the Pathogenesis of Cardiovascular Diseases
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Role of Mitochondrial Dysfunction in the Pathogenesis of Cardiovascular Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 June 2021) | Viewed by 12506

Special Issue Editors

Dr. Speranza Rubattu

E-Mail Website
Guest Editor
1. IRCCS Neuromed, 86077 Pozzilli, Italy
2. Department of Clinical and Molecular Medicine, School of Medicine and Psychology, Sapienza University, 00185 Rome, Italy
Interests: cardiovascular medicine
Special Issues, Collections and Topics in MDPI journals
Dr. Maurizio Forte

E-Mail Website
Co-Guest Editor
Department of Angio-Cardio-Neurology, IRCCS Neuromed, 86077 Pozzilli, Italy
Interests: cardiovascular diseases; autophagy; nutraceuticals; stroke; mitochondrial dysfunction
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiovascular diseases (CVDs) are common multifactorial pathological conditions that affect a large proportion of the general population in each country, with a heavy burden for the national health systems.

There is a need to improve our knowledge of the complex etiopathogenesis of CVDs. Unfortunately, despite several efforts performed over the last decades, still much remains to be identified.

Mitochondria are essential organelles in the life of cells. Mitochondrial dysfunction, an abnormal condition that alters cell integrity and function, contributes to several diseases. The contribution of this molecular mechanism to the pathogenesis of CVDs has been understood more recently and is currently being explored in deeper detail in different experimental set ups. The full comprehension of the contribution of mitochondrial dysfunction to CVD pathogenesis will allow the identification of novel targets that are able to improve the prevention, diagnosis, and treatment of CVDs. In fact, novel therapeutic strategies, counteracting mitochondrial dysfunction, have been already designed and are currently being tested, with promising results.

This Special Issue will collect original papers and review articles focused on the role of mitochondrial dysfunction in different CVDs, including hypertension and target organ damage, cardiomiopaties, ischemic heart disease, stroke, heart failure, and cardiorenal syndrome.

A focus on the pathogenic mechanistic contribution, as well as on the prevention and treatment of CVDs through new approaches that are able to counteract mitochondrial dysfunction, will be a relevant aspect of this Issue.

Overall, the main goal of this Special Issue of the International Journal of Molecular Sciences will be a comprehensive overview of the state of the art on this important matter.

Dr. Speranza Rubattu
Dr. Maurizio Forte
Guest Editors

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.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Published Papers (4 papers)

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Research

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15 pages, 4557 KiB  
Article
Long-Chain Acyl-Carnitines Interfere with Mitochondrial ATP Production Leading to Cardiac Dysfunction in Zebrafish
by Deung-Dae Park, Bernd M. Gahr, Julia Krause, Wolfgang Rottbauer, Tanja Zeller and Steffen Just
Int. J. Mol. Sci. 2021, 22(16), 8468; https://doi.org/10.3390/ijms22168468 - 06 Aug 2021
Cited by 5 | Viewed by 2169
Abstract
In the human heart, the energy supplied by the production of ATP is predominately accomplished by ß-oxidation in mitochondria, using fatty acids (FAs) as the primary fuel. Long-chain acylcarnitines (LCACs) are intermediate forms of FA transport that are essential for FA delivery from [...] Read more.
In the human heart, the energy supplied by the production of ATP is predominately accomplished by ß-oxidation in mitochondria, using fatty acids (FAs) as the primary fuel. Long-chain acylcarnitines (LCACs) are intermediate forms of FA transport that are essential for FA delivery from the cytosol into mitochondria. Here, we analyzed the impact of the LCACs C18 and C18:1 on mitochondrial function and, subsequently, on heart functionality in the in vivo vertebrate model system of zebrafish (Danio rerio). Since LCACs are formed and metabolized in mitochondria, we assessed mitochondrial morphology, structure and density in C18- and C18:1-treated zebrafish and found no mitochondrial alterations compared to control-treated (short-chain acylcarnitine, C3) zebrafish embryos. However, mitochondrial function and subsequently ATP production was severely impaired in C18- and C18:1-treated zebrafish embryos. Furthermore, we found that C18 and C18:1 treatment of zebrafish embryos led to significantly impaired cardiac contractile function, accompanied by reduced heart rate and diminished atrial and ventricular fractional shortening, without interfering with cardiomyocyte differentiation, specification and growth. In summary, our findings provide insights into the direct role of long-chain acylcarnitines on vertebrate heart function by interfering with regular mitochondrial function and thereby energy allocation in cardiomyocytes. Full article
(This article belongs to the Special Issue Role of Mitochondrial Dysfunction in the Pathogenesis of Cardiovascular Diseases)
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14 pages, 2837 KiB  
Article
Complex III Inhibition-Induced Pulmonary Hypertension Affects the Mitochondrial Proteomic Landscape
by Joel James, Mathews Valuparampil Varghese, Mikhail Vasilyev, Paul R. Langlais, Stevan P. Tofovic, Olga Rafikova and Ruslan Rafikov
Int. J. Mol. Sci. 2020, 21(16), 5683; https://doi.org/10.3390/ijms21165683 - 08 Aug 2020
Cited by 11 | Viewed by 3157
Abstract
The mitochondria play a vital role in controlling cell metabolism and regulating crucial cellular outcomes. We previously demonstrated that chronic inhibition of the mitochondrial complex III in rats by Antimycin A (AA) induced sustained pulmonary vasoconstriction. On the metabolic level, AA-induced mitochondrial dysfunction [...] Read more.
The mitochondria play a vital role in controlling cell metabolism and regulating crucial cellular outcomes. We previously demonstrated that chronic inhibition of the mitochondrial complex III in rats by Antimycin A (AA) induced sustained pulmonary vasoconstriction. On the metabolic level, AA-induced mitochondrial dysfunction resulted in a glycolytic shift that was reported as the primary contributor to pulmonary hypertension pathogenesis. However, the regulatory proteins driving this metabolic shift with complex III inhibition are yet to be explored. Therefore, to delineate the mechanisms, we followed changes in the rat lung mitochondrial proteome throughout AA treatment. Rats treated with AA for up to 24 days showed a disturbed mitochondrial proteome with significant changes in 28 proteins (p < 0.05). We observed a time-dependent decrease in the expression of key proteins that regulate fatty acid oxidation, the tricarboxylic acid cycle, the electron transport chain, and amino acid metabolism, indicating a correlation with diminished mitochondrial function. We also found a significant dysregulation in proteins that controls the protein import machinery and the clearance and detoxification of oxidatively damaged peptides via proteolysis and mitophagy. This could potentially lead to the onset of mitochondrial toxicity due to misfolded protein stress. We propose that chronic inhibition of mitochondrial complex III attenuates mitochondrial function by disruption of the global mitochondrial metabolism. This potentially aggravates cellular proliferation by initiating a glycolytic switch and thereby leads to pulmonary hypertension. Full article
(This article belongs to the Special Issue Role of Mitochondrial Dysfunction in the Pathogenesis of Cardiovascular Diseases)
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Review

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16 pages, 761 KiB  
Review
Profilin 1 and Mitochondria—Partners in the Pathogenesis of Coronary Artery Disease?
by Elżbieta Paszek, Wojciech Zajdel, Tomasz Rajs, Krzysztof Żmudka, Jacek Legutko and Paweł Kleczyński
Int. J. Mol. Sci. 2021, 22(3), 1100; https://doi.org/10.3390/ijms22031100 - 22 Jan 2021
Cited by 9 | Viewed by 2469
Abstract
Atherosclerosis remains a large health and economic burden. Even though it has been studied for more than a century, its complex pathophysiology has not been elucidated. The relatively well-established contributors include: chronic inflammation in response to oxidized cholesterol, reactive oxygen species-induced damage and [...] Read more.
Atherosclerosis remains a large health and economic burden. Even though it has been studied for more than a century, its complex pathophysiology has not been elucidated. The relatively well-established contributors include: chronic inflammation in response to oxidized cholesterol, reactive oxygen species-induced damage and apoptosis. Recently, profilin 1, a regulator of actin dynamics emerged as a potential new player in the field. Profilin is abundant in stable atherosclerotic plaques and in thrombi extracted from infarct-related arteries in patients with acute myocardial infarction. The exact role of profilin in atherosclerosis and its complications, as well as its mechanisms of action, remain unknown. Here, we summarize several pathways in which profilin may act through mitochondria in a number of processes implicated in atherosclerosis. Full article
(This article belongs to the Special Issue Role of Mitochondrial Dysfunction in the Pathogenesis of Cardiovascular Diseases)
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24 pages, 2660 KiB  
Review
Aortic Valve Stenosis and Mitochondrial Dysfunctions: Clinical and Molecular Perspectives
by Gaia Pedriali, Giampaolo Morciano, Simone Patergnani, Paolo Cimaglia, Cristina Morelli, Elisa Mikus, Roberto Ferrari, Vincenzo Gasbarro, Carlotta Giorgi, Mariusz R. Wieckowski and Paolo Pinton
Int. J. Mol. Sci. 2020, 21(14), 4899; https://doi.org/10.3390/ijms21144899 - 11 Jul 2020
Cited by 19 | Viewed by 4204
Abstract
Calcific aortic stenosis is a disorder that impacts the physiology of heart valves. Fibrocalcific events progress in conjunction with thickening of the valve leaflets. Over the years, these events promote stenosis and obstruction of blood flow. Known and common risk factors are congenital [...] Read more.
Calcific aortic stenosis is a disorder that impacts the physiology of heart valves. Fibrocalcific events progress in conjunction with thickening of the valve leaflets. Over the years, these events promote stenosis and obstruction of blood flow. Known and common risk factors are congenital defects, aging and metabolic syndromes linked to high plasma levels of lipoproteins. Inflammation and oxidative stress are the main molecular mediators of the evolution of aortic stenosis in patients and these mediators regulate both the degradation and remodeling processes. Mitochondrial dysfunction and dysregulation of autophagy also contribute to the disease. A better understanding of these cellular impairments might help to develop new ways to treat patients since, at the moment, there is no effective medical treatment to diminish neither the advancement of valve stenosis nor the left ventricular function impairments, and the current approaches are surgical treatment or transcatheter aortic valve replacement with prosthesis. Full article
(This article belongs to the Special Issue Role of Mitochondrial Dysfunction in the Pathogenesis of Cardiovascular Diseases)
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