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Special Issue "Bioenergetics, Mitochondrial Dynamics and Cardiac Disease"

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: 31 December 2021.

Special Issue Editors

Prof. Antigone Lazou
E-Mail Website
Guest Editor
School of Biology, Aristotle University of Thessaloniki, Thessaloniki 54124, Greece
Interests: molecular mechanisms underlying cardiac dysfunction in disease; ischemia/reperfusion injury; heart failure; oxidative stress; intracellular signaling; redox signaling; metabolic regulation; mitochondrial function.
Dr. Chrishan J.A. Ramachandra
E-Mail
Guest Editor
National Heart Research Institute Singapore, National Heart Centre Singapore, 5 Hospital Drive, Singapore 169609
Interests: induced pluripotent stem cells (iPSCs); cardiovascular disease modeling and drug discovery; cardiometabolic disorders; cardiac bioenergetics; cell signaling and transcription factors in cardiogenesis.

Special Issue Information

Dear Colleagues,

Cardiovascular diseases remain the leading cause of death and disability worldwide despite the progress made over the past three decades in the prevention, diagnosis, and management of the disease. Thus, there is a substantial need to find novel approaches that could specifically address repair and regeneration of damaged and/or lost myocardium.

Cardiac disease is associated with metabolic changes that cause a progressive impairment of cardiac muscle high-energy phosphate production with further maladaptive effects. Advances in animal models and systems-based approaches have revealed that mitochondria have diverse functions beyond bioenergetics, and the ability to adapt and respond to a plethora of cellular and tissue-specific stimuli. Mitochondrial dysfunction has been identified as a key perturbation underlying numerous pathologies including heart failure and metabolic disorders. Emerging evidence highlights the connection between mitochondrial biology and changes in cardiac metabolism and their importance for cell survival and/or the progress of cardiac pathology.

This Special Issue will bring together reviews and original articles addressing the molecular signaling that connects metabolism and energy-sensing with mitochondrial function, and the roles of basic mitochondrial processes in metabolism and cardiac dysfunction. Identification of therapeutic targets and the development of novel approaches to treat cardiac diseases will be also a relevant aspect of this issue.

Prof. Antigone Lazou
Dr. Chrishan J.A. Ramachandra
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 papers will be 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.

Keywords

  • Cardiomyopathies
  • Heart failure
  • Ischemia/reperfusion injury
  • Myocardial infarction
  • Oxidative stress
  • Cell metabolism
  • Metabolic diseases
  • Energy homeostasis
  • Mitochondrial dynamics
  • mitochondrial fusion
  • mitochondrial fission
  • mitophagy
  • mitochondrial biogenesis

Published Papers (5 papers)

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Research

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Article
Cardioprotective Effects of PPARβ/δ Activation against Ischemia/Reperfusion Injury in Rat Heart Are Associated with ALDH2 Upregulation, Amelioration of Oxidative Stress and Preservation of Mitochondrial Energy Production
Int. J. Mol. Sci. 2021, 22(12), 6399; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22126399 - 15 Jun 2021
Viewed by 716
Abstract
Accumulating evidence support the cardioprotective properties of the nuclear receptor peroxisome proliferator activated receptor β/δ (PPARβ/δ); however, the underlying mechanisms are not yet fully elucidated. The aim of the study was to further investigate the mechanisms underlying PPARβ/δ-mediated cardioprotection in the setting of [...] Read more.
Accumulating evidence support the cardioprotective properties of the nuclear receptor peroxisome proliferator activated receptor β/δ (PPARβ/δ); however, the underlying mechanisms are not yet fully elucidated. The aim of the study was to further investigate the mechanisms underlying PPARβ/δ-mediated cardioprotection in the setting of myocardial ischemia/reperfusion (I/R). For this purpose, rats were treated with PPARβ/δ agonist GW0742 and/or antagonist GSK0660 in vivo and hearts were subjected to ex vivo global ischemia followed by reperfusion. PPARβ/δ activation improved left ventricular developed pressure recovery, reduced infarct size (IS) and incidence of reperfusion-induced ventricular arrhythmias while it also up-regulated superoxide dismutase 2, catalase and uncoupling protein 3 resulting in attenuation of oxidative stress as evidenced by the reduction in 4-hydroxy-2-nonenal protein adducts and protein carbonyl formation. PPARβ/δ activation also increased both mRNA expression and enzymatic activity of aldehyde dehydrogenase 2 (ALDH2); inhibition of ALDH2 abrogated the IS limiting effect of PPARβ/δ activation. Furthermore, upregulation of PGC-1α and isocitrate dehydrogenase 2 mRNA expression, increased citrate synthase activity as well as mitochondrial ATP content indicated improvement in mitochondrial content and energy production. These data provide new mechanistic insight into the cardioprotective properties of PPARβ/δ in I/R pointing to ALDH2 as a direct downstream target and suggesting that PPARβ/δ activation alleviates myocardial I/R injury through coordinated stimulation of the antioxidant defense of the heart and preservation of mitochondrial function. Full article
(This article belongs to the Special Issue Bioenergetics, Mitochondrial Dynamics and Cardiac Disease)
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Article
Lack of Contribution of p66shc to Pressure Overload-Induced Right Heart Hypertrophy
Int. J. Mol. Sci. 2020, 21(24), 9339; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21249339 - 08 Dec 2020
Cited by 2 | Viewed by 610
Abstract
The leading cause of death in pulmonary arterial hypertension (PAH) is right ventricular (RV) failure (RVF). Reactive oxygen species (ROS) have been suggested to play a role in the development of RV hypertrophy (RVH) and the transition to RVF. The hydrogen peroxide-generating protein [...] Read more.
The leading cause of death in pulmonary arterial hypertension (PAH) is right ventricular (RV) failure (RVF). Reactive oxygen species (ROS) have been suggested to play a role in the development of RV hypertrophy (RVH) and the transition to RVF. The hydrogen peroxide-generating protein p66shc has been associated with left ventricular (LV) hypertrophy but its role in RVH is unclear. The purpose of this study was to determine whether genetic deletion of p66shc affects the development and/or progression of RVH and RVF in the pulmonary artery banding (PAB) model of RV pressure overload. The impact of p66shc on mitochondrial ROS formation, RV cardiomyocyte function, as well as on RV morphology and function were studied three weeks after PAB or sham operation. PAB in wild type mice did not affect mitochondrial ROS production or RV cardiomyocyte function, but induced RVH and impaired cardiac function. Genetic deletion of p66shc did also not alter basal mitochondrial ROS production or RV cardiomyocyte function, but impaired RV cardiomyocyte shortening was observed following PAB. The development of RVH and RVF following PAB was not affected by p66shc deletion. Thus, our data suggest that p66shc-derived ROS are not involved in the development and progression of RVH or RVF in PAH. Full article
(This article belongs to the Special Issue Bioenergetics, Mitochondrial Dynamics and Cardiac Disease)
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Article
Fingolimod (FTY720) Preserves High Energy Phosphates and Improves Cardiac Function in Heterotopic Heart Transplantation Model
Int. J. Mol. Sci. 2020, 21(18), 6548; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21186548 - 08 Sep 2020
Cited by 1 | Viewed by 802
Abstract
During heart transplantation, donor heart leads to reduced oxygen supply resulting in low level of high energy phosphate (HEP) reserves in cardiomyocyte. Lower HEP is one of the underlying reasons of cell death due to ischemia. In this study we investigated the role [...] Read more.
During heart transplantation, donor heart leads to reduced oxygen supply resulting in low level of high energy phosphate (HEP) reserves in cardiomyocyte. Lower HEP is one of the underlying reasons of cell death due to ischemia. In this study we investigated the role of Fingolimod (FTY720) in heart transplantation ischemia. Eight groups of Sprague-Dawley rats (n = 5 for each subgroup) were made, A1 and C1 were given FTY720 1 mg/kg while B1 and D1 were given normal saline. The hearts were implanted into another set of similar rats after preservation period of 1 h at 4–8 °C. Significantly higher Left ventricular systolic pressure (LVSP), dP/dT maximum (p < 0.05), dP/dT minimum (p < 0.05) were recorded in the FTY720 treated group after 24 h of reperfusion while after 1 h of reperfusion, there were no significant differences in LVSP, maximum and negative dP/dT, and Left ventricular end diastolic pressure (LVEDP) between the control and the FTY720-treated transplant groups. Coronary blood flow (CBF) was enhanced (p < 0.05) in the FTY720 treated group after 1 and 24 h. ATP p < 0.001, p < 0.05 at 1 and 24 h, ADP p < 0.001, p > 0.05 at 1 and 24 h, and phosphocreatine p < 0.05, p > 0.05 at 1 and 24 h were better preserved by FTY720 treatment as compared to control group. The study concluded that pretreatment of grafted hearts with FTY720 improved hemodynamics, CBF, high energy phosphate reserves, reduces the peroxynitrite level and poly (ADP ribose) polymerase (PARP) inhibition that prevents ischemia-reperfusion injury. Full article
(This article belongs to the Special Issue Bioenergetics, Mitochondrial Dynamics and Cardiac Disease)
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Review

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Review
Mitochondrial Homeostasis Mediates Lipotoxicity in the Failing Myocardium
Int. J. Mol. Sci. 2021, 22(3), 1498; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22031498 - 02 Feb 2021
Viewed by 1033
Abstract
Heart failure remains the most common cause of death in the industrialized world. In spite of new therapeutic interventions that are constantly being developed, it is still not possible to completely protect against heart failure development and progression. This shows how much more [...] Read more.
Heart failure remains the most common cause of death in the industrialized world. In spite of new therapeutic interventions that are constantly being developed, it is still not possible to completely protect against heart failure development and progression. This shows how much more research is necessary to understand the underlying mechanisms of this process. In this review, we give a detailed overview of the contribution of impaired mitochondrial dynamics and energy homeostasis during heart failure progression. In particular, we focus on the regulation of fatty acid metabolism and the effects of fatty acid accumulation on mitochondrial structural and functional homeostasis. Full article
(This article belongs to the Special Issue Bioenergetics, Mitochondrial Dynamics and Cardiac Disease)
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Review
Mitochondrial Dysfunction and Heart Disease: Critical Appraisal of an Overlooked Association
Int. J. Mol. Sci. 2021, 22(2), 614; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22020614 - 09 Jan 2021
Cited by 2 | Viewed by 1195
Abstract
The myocardium is among the most energy-consuming tissues in the body, burning from 6 to 30 kg of ATP per day within the mitochondria, the so-called powerhouse of the cardiomyocyte. Although mitochondrial genetic disorders account for a small portion of cardiomyopathies, mitochondrial dysfunction [...] Read more.
The myocardium is among the most energy-consuming tissues in the body, burning from 6 to 30 kg of ATP per day within the mitochondria, the so-called powerhouse of the cardiomyocyte. Although mitochondrial genetic disorders account for a small portion of cardiomyopathies, mitochondrial dysfunction is commonly involved in a broad spectrum of heart diseases, and it has been implicated in the development of heart failure via maladaptive circuits producing and perpetuating mitochondrial stress and energy starvation. In this bench-to-bedside review, we aimed to (i) describe the key functions of the mitochondria within the myocardium, including their role in ischemia/reperfusion injury and intracellular calcium homeostasis; (ii) examine the contribution of mitochondrial dysfunction to multiple cardiac disease phenotypes and their transition to heart failure; and (iii) discuss the rationale and current evidence for targeting mitochondrial function for the treatment of heart failure, including via sodium-glucose cotransporter 2 inhibitors. Full article
(This article belongs to the Special Issue Bioenergetics, Mitochondrial Dynamics and Cardiac Disease)
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