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Cardiovascular Pharmacology and Interventions: Future Directions for Cardioprotection
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Cardiovascular Pharmacology and Interventions: Future Directions for Cardioprotection

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

Deadline for manuscript submissions: closed (30 March 2022) | Viewed by 18030

Special Issue Editors

Dr. Bijan Ghaleh

E-Mail
Guest Editor
INSERM U 955 Equipe 03, Faculté de Médecine, Creteil Medical School and Veterinary School of Alfort, 94000 Créteil, France
Interests: cardiovascular pharmacology; coronary circulation; myocardial ischemia and infarction; heart failure
Special Issues, Collections and Topics in MDPI journals
Dr. Speranza Rubattu

E-Mail Website
Co-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. Alessandro Di Minno

E-Mail Website
Co-Guest Editor
Department of Pharmacy, Università degli Studi di Napoli Federico II, Naples, Italy
Interests: oxidative stress; cardiovascular disease; reactive oxygen species; pharmacological treatment
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Despite major advances in cardiology and the prevention of cardiovascular diseases, myocardial infarction remains one of the leading causes of mortality worldwide, especially in relation to the increasing incidence of diabetes and obesity. While the degree of necrosis, the severity of reverse remodeling, and the prognosis of myocardial infarction have been dramatically improved by the use of rapid reperfusion strategies, the mortality rate in the year following myocardial infarction is still high and the transition to long-term heart failure remains a major concern. This Special Issue “Cardiovascular Pharmacology and Interventions: Future Directions for Cardioprotection” aims to stimulate comprehensive research in this field. We will accept articles on the pathophysiology of myocardial infarction and post-myocardial infarction remodeling, molecular basis, imaging, and cardioprotective strategies including pharmacological and non-pharmacological approaches.

Dr. Bijan Ghaleh
Dr. Speranza Rubattu
Dr. Alessandro Di Minno
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.

Keywords

  • cardiovascular pharmacology
  • coronary circulation
  • myocardial ischemia and infarction
  • heart failure

Related Special Issue

Published Papers (5 papers)

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Research

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11 pages, 2249 KiB  
Article
Cardioprotective Signaling Pathways in Obese Mice Submitted to Regular Exercise: Effect on Oxysterols
by Caroline Barau, Shirin Leick, Claudio Caccia, Lolita Portal, Valerio Leoni, Philippe Le Corvoisier, Didier Morin, Bijan Ghaleh and Sandrine Pons
Int. J. Mol. Sci. 2022, 23(18), 10840; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms231810840 - 16 Sep 2022
Cited by 2 | Viewed by 1470
Abstract
Exercise induces cardioprotection against myocardial infarction, despite obesity, by restoring pro-survival pathways and increasing resistance of mitochondrial permeability transition pore (mPTP) opening at reperfusion. Among the mechanisms involved in the inactivation of these pathways, oxysterols appear interesting. Thus, we investigated the influence of [...] Read more.
Exercise induces cardioprotection against myocardial infarction, despite obesity, by restoring pro-survival pathways and increasing resistance of mitochondrial permeability transition pore (mPTP) opening at reperfusion. Among the mechanisms involved in the inactivation of these pathways, oxysterols appear interesting. Thus, we investigated the influence of regular exercise on the reperfusion injury salvage kinase (RISK) pathway, oxysterols, and mitochondria, in the absence of ischemia-reperfusion. We also studied 7β-hydroxycholesterol (7βOH) concentration (mass spectrometry) in human lean and obese subjects. Wild-type (WT) and obese (ob/ob) mice were assigned to sedentary conditions or regular treadmill exercise. Exercise significantly increased Akt phosphorylation, whereas 7βOH concentration was reduced. Moreover, exercise induced the translocation of PKCε from the cytosol to mitochondria. However, exercise did not affect the calcium concentration required to open mPTP in the mitochondria, neither in WT nor in ob/ob animals. Finally, human plasma 7βOH concentration was consistent with observations made in mice. In conclusion, regular exercise enhanced the RISK pathway by increasing kinase phosphorylation and PKCε translocation and decreasing 7βOH concentration. This activation needs the combination with stress conditions, i.e., ischemia-reperfusion, in order to inhibit mPTP opening at the onset of reperfusion. The human findings suggest 7βOH as a candidate marker for evaluating cardiovascular risk factors in obesity. Full article
(This article belongs to the Special Issue Cardiovascular Pharmacology and Interventions: Future Directions for Cardioprotection)
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18 pages, 4256 KiB  
Article
Phosphatidylserine Supplementation as a Novel Strategy for Reducing Myocardial Infarct Size and Preventing Adverse Left Ventricular Remodeling
by David Schumacher, Adelina Curaj, Mareike Staudt, Franziska Cordes, Andreea R. Dumitraşcu, Benjamin Rolles, Christian Beckers, Josefin Soppert, Mihaela Rusu, Sakine Simsekyilmaz, Kinan Kneizeh, Chrishan J. A. Ramachandra, Derek J. Hausenloy and Elisa A. Liehn
Int. J. Mol. Sci. 2021, 22(9), 4401; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094401 - 22 Apr 2021
Cited by 10 | Viewed by 3523
Abstract
Phosphatidylserines are known to sustain skeletal muscle activity during intense activity or hypoxic conditions, as well as preserve neurocognitive function in older patients. Our previous studies pointed out a potential cardioprotective role of phosphatidylserine in heart ischemia. Therefore, we investigated the effects of [...] Read more.
Phosphatidylserines are known to sustain skeletal muscle activity during intense activity or hypoxic conditions, as well as preserve neurocognitive function in older patients. Our previous studies pointed out a potential cardioprotective role of phosphatidylserine in heart ischemia. Therefore, we investigated the effects of phosphatidylserine oral supplementation in a mouse model of acute myocardial infarction (AMI). We found out that phosphatidylserine increases, significantly, the cardiomyocyte survival by 50% in an acute model of myocardial ischemia-reperfusion. Similar, phosphatidylserine reduced significantly the infarcted size by 30% and improved heart function by 25% in a chronic model of AMI. The main responsible mechanism seems to be up-regulation of protein kinase C epsilon (PKC-ε), the main player of cardio-protection during pre-conditioning. Interestingly, if the phosphatidylserine supplementation is started before induction of AMI, but not after, it selectively inhibits neutrophil’s activation, such as Interleukin 1 beta (IL-1β) expression, without affecting the healing and fibrosis. Thus, phosphatidylserine supplementation may represent a simple way to activate a pre-conditioning mechanism and may be a promising novel strategy to reduce infarct size following AMI and to prevent myocardial injury during myocardial infarction or cardiac surgery. Due to the minimal adverse effects, further investigation in large animals or in human are soon possible to establish the exact role of phosphatidylserine in cardiac diseases. Full article
(This article belongs to the Special Issue Cardiovascular Pharmacology and Interventions: Future Directions for Cardioprotection)
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11 pages, 1900 KiB  
Article
Argon Attenuates Multiorgan Failure in Relation with HMGB1 Inhibition
by Quentin de Roux, Fanny Lidouren, Agathe Kudela, Lina Slassi, Matthias Kohlhauer, Emilie Boissady, Matthieu Chalopin, Géraldine Farjot, Catherine Billoet, Patrick Bruneval, Bijan Ghaleh, Nicolas Mongardon and Renaud Tissier
Int. J. Mol. Sci. 2021, 22(6), 3257; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22063257 - 23 Mar 2021
Cited by 5 | Viewed by 2113
Abstract
Argon inhalation attenuates multiorgan failure (MOF) after experimental ischemic injury. We hypothesized that this protection could involve decreased High Mobility Group Box 1 (HMGB1) systemic release. We investigated this issue in an animal model of MOF induced by aortic cross-clamping. Anesthetized rabbits were [...] Read more.
Argon inhalation attenuates multiorgan failure (MOF) after experimental ischemic injury. We hypothesized that this protection could involve decreased High Mobility Group Box 1 (HMGB1) systemic release. We investigated this issue in an animal model of MOF induced by aortic cross-clamping. Anesthetized rabbits were submitted to supra-coeliac aortic cross-clamping for 30 min, followed by 300 min of reperfusion. They were randomly divided into three groups (n = 7/group). The Control group inhaled nitrogen (70%) and oxygen (30%). The Argon group was exposed to a mixture of argon (70%) and oxygen (30%). The last group inhaled nitrogen/oxygen (70/30%) with an administration of the HMGB1 inhibitor glycyrrhizin (4 mg/kg i.v.) 5 min before aortic unclamping. At the end of follow-up, cardiac output was significantly higher in Argon and Glycyrrhizin vs. Control (60 ± 4 and 49 ± 4 vs. 33 ± 8 mL/kg/min, respectively). Metabolic acidosis was attenuated in Argon and Glycyrrhizin vs. Control, along with reduced amount of norepinephrine to reverse arterial hypotension. This was associated with reduced interleukin-6 and HMGB1 plasma concentration in Argon and Glycyrrhizin vs. Control. End-organ damages were also attenuated in the liver and kidney in Argon and Glycyrrhizin vs. Control, respectively. Argon inhalation reduced HMGB1 blood level after experimental aortic cross-clamping and provided similar benefits to direct HMGB1 inhibition. Full article
(This article belongs to the Special Issue Cardiovascular Pharmacology and Interventions: Future Directions for Cardioprotection)
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Review

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20 pages, 2177 KiB  
Review
Immune and Inflammatory Networks in Myocardial Infarction: Current Research and Its Potential Implications for the Clinic
by Atsushi Anzai, Seien Ko and Keiichi Fukuda
Int. J. Mol. Sci. 2022, 23(9), 5214; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23095214 - 06 May 2022
Cited by 16 | Viewed by 5042
Abstract
Despite recent scientific and technological advances, myocardial infarction (MI) still represents a major global health problem, leading to high morbidity and mortality worldwide. During the post-MI wound healing process, dysregulated immune inflammatory pathways and failure to resolve inflammation are associated with maladaptive left [...] Read more.
Despite recent scientific and technological advances, myocardial infarction (MI) still represents a major global health problem, leading to high morbidity and mortality worldwide. During the post-MI wound healing process, dysregulated immune inflammatory pathways and failure to resolve inflammation are associated with maladaptive left ventricular remodeling, progressive heart failure, and eventually poor outcomes. Given the roles of immune cells in the host response against tissue injury, understanding the involved cellular subsets, sources, and functions is essential for discovering novel therapeutic strategies that preserve the protective immune system and promote optimal healing. This review discusses the cellular effectors and molecular signals across multi-organ systems, which regulate the inflammatory and reparative responses after MI. Additionally, we summarize the recent clinical and preclinical data that propel conceptual revolutions in cardiovascular immunotherapy. Full article
(This article belongs to the Special Issue Cardiovascular Pharmacology and Interventions: Future Directions for Cardioprotection)
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16 pages, 374 KiB  
Review
Challenges in Metabolomics-Based Tests, Biomarkers Revealed by Metabolomic Analysis, and the Promise of the Application of Metabolomics in Precision Medicine
by Alessandro Di Minno, Monica Gelzo, Marianna Caterino, Michele Costanzo, Margherita Ruoppolo and Giuseppe Castaldo
Int. J. Mol. Sci. 2022, 23(9), 5213; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23095213 - 06 May 2022
Cited by 29 | Viewed by 4825
Abstract
Metabolomics helps identify metabolites to characterize/refine perturbations of biological pathways in living organisms. Pre-analytical, analytical, and post-analytical limitations that have hampered a wide implementation of metabolomics have been addressed. Several potential biomarkers originating from current targeted metabolomics-based approaches have been discovered. Precision medicine [...] Read more.
Metabolomics helps identify metabolites to characterize/refine perturbations of biological pathways in living organisms. Pre-analytical, analytical, and post-analytical limitations that have hampered a wide implementation of metabolomics have been addressed. Several potential biomarkers originating from current targeted metabolomics-based approaches have been discovered. Precision medicine argues for algorithms to classify individuals based on susceptibility to disease, and/or by response to specific treatments. It also argues for a prevention-based health system. Because of its ability to explore gene–environment interactions, metabolomics is expected to be critical to personalize diagnosis and treatment. Stringent guidelines have been applied from the very beginning to design studies to acquire the information currently employed in precision medicine and precision prevention approaches. Large, prospective, expensive and time-consuming studies are now mandatory to validate old, and discover new, metabolomics-based biomarkers with high chances of translation into precision medicine. Metabolites from studies on saliva, sweat, breath, semen, feces, amniotic, cerebrospinal, and broncho-alveolar fluid are predicted to be needed to refine information from plasma and serum metabolome. In addition, a multi-omics data analysis system is predicted to be needed for omics-based precision medicine approaches. Omics-based approaches for the progress of precision medicine and prevention are expected to raise ethical issues. Full article
(This article belongs to the Special Issue Cardiovascular Pharmacology and Interventions: Future Directions for Cardioprotection)
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