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Cardiovascular Injuries in Severe Respiratory Infectious Diseases 2.0
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Cardiovascular Injuries in Severe Respiratory Infectious Diseases 2.0

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 (31 March 2022) | Viewed by 8720

Special Issue Editors

Dr. Atsushi Tanaka

E-Mail Website
Guest Editor
Department of Cardiovascular Medicine, Saga University, Saga, Japan
Interests: cardio-metabolic syndrome; preventive cardiology; clinical trial; vascular medicine; heart failure
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Koichi Node

E-Mail Website
Guest Editor
Department of Cardiovascular Medicine, Saga University, Saga, Japan
Interests: heart failure; hypertension; atherosclerosis; vascular disease; heart disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

According to recently accumulated evidence, substantial deaths of individuals infected by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) proved to be explained by fatal nonrespiratory conditions, such as cardiovascular-related complications. However, detailed mechanisms of cardiovascular injuries in several severe respiratory infectious diseases, including coronavirus disease 19 (COVID-19) and SARS-CoV-2, is still limited. To predict and prevent the risk of such cardiovascular injuries and complications in patients with severe respiratory infectious diseases, it would be pivotal to elucidate in more detail the molecular mechanisms by which severe respiratory infectious diseases can damage the cardiovascular system and cause cardiovascular complications. This second release of the Special Issue topic continues to welcome mechanical, experimental, and translational studies widely addressing this hot topic. Importantly, when considering your submission, please keep in mind that IJMS is a journal of molecular science. This Special Issue is not limited to the COVID-19 and SARS-CoV-2. Articles, full reviews and communications are welcome contributions to our Special Issue.

Dr. Atsushi Tanaka
Prof. Dr. Koichi Node
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.

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Keywords

  • severe respiratory infectious diseases
  • cardiovascular disease
  • COVID-19
  • SARS-CoV-2

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Published Papers (3 papers)

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Editorial

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3 pages, 175 KiB  
Editorial
Collective Knowledge Used to Unveil Cardiovascular Injury Emerged during COVID-19
by Atsushi Tanaka and Koichi Node
Int. J. Mol. Sci. 2022, 23(9), 5178; https://doi.org/10.3390/ijms23095178 - 6 May 2022
Viewed by 1093
Abstract
Two years have passed since the unprecedented breakout of the global pandemic of the coronavirus disease COVID-19, which began at the end of 2019 [...] Full article
(This article belongs to the Special Issue Cardiovascular Injuries in Severe Respiratory Infectious Diseases 2.0)

Research

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17 pages, 3650 KiB  
Article
Mechanism of Blood–Heart-Barrier Leakage: Implications for COVID-19 Induced Cardiovascular Injury
by Rubens P. Homme, Akash K. George, Mahavir Singh, Irina Smolenkova, Yuting Zheng, Sathnur Pushpakumar and Suresh C. Tyagi
Int. J. Mol. Sci. 2021, 22(24), 13546; https://doi.org/10.3390/ijms222413546 - 17 Dec 2021
Cited by 9 | Viewed by 2993
Abstract
Although blood–heart-barrier (BHB) leakage is the hallmark of congestive (cardio-pulmonary) heart failure (CHF), the primary cause of death in elderly, and during viral myocarditis resulting from the novel coronavirus variants such as the severe acute respiratory syndrome novel corona virus 2 (SARS-CoV-2) known [...] Read more.
Although blood–heart-barrier (BHB) leakage is the hallmark of congestive (cardio-pulmonary) heart failure (CHF), the primary cause of death in elderly, and during viral myocarditis resulting from the novel coronavirus variants such as the severe acute respiratory syndrome novel corona virus 2 (SARS-CoV-2) known as COVID-19, the mechanism is unclear. The goal of this project is to determine the mechanism of the BHB in CHF. Endocardial endothelium (EE) is the BHB against leakage of blood from endocardium to the interstitium; however, this BHB is broken during CHF. Previous studies from our laboratory, and others have shown a robust activation of matrix metalloproteinase-9 (MMP-9) during CHF. MMP-9 degrades the connexins leading to EE dysfunction. We demonstrated juxtacrine coupling of EE with myocyte and mitochondria (Mito) but how it works still remains at large. To test whether activation of MMP-9 causes EE barrier dysfunction, we hypothesized that if that were the case then treatment with hydroxychloroquine (HCQ) could, in fact, inhibit MMP-9, and thus preserve the EE barrier/juxtacrine signaling, and synchronous endothelial-myocyte coupling. To determine this, CHF was created by aorta-vena cava fistula (AVF) employing the mouse as a model system. The sham, and AVF mice were treated with HCQ. Cardiac hypertrophy, tissue remodeling-induced mitochondrial-myocyte, and endothelial-myocyte contractions were measured. Microvascular leakage was measured using FITC-albumin conjugate. The cardiac function was measured by echocardiography (Echo). Results suggest that MMP-9 activation, endocardial endothelial leakage, endothelial-myocyte (E-M) uncoupling, dyssynchronous mitochondrial fusion-fission (Mfn2/Drp1 ratio), and mito-myocyte uncoupling in the AVF heart failure were found to be rampant; however, treatment with HCQ successfully mitigated some of the deleterious cardiac alterations during CHF. The findings have direct relevance to the gamut of cardiac manifestations, and the resultant phenotypes arising from the ongoing complications of COVID-19 in human subjects. Full article
(This article belongs to the Special Issue Cardiovascular Injuries in Severe Respiratory Infectious Diseases 2.0)
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Review

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25 pages, 2791 KiB  
Review
Pathogenic Basis of Thromboinflammation and Endothelial Injury in COVID-19: Current Findings and Therapeutic Implications
by Yasutomi Higashikuni, Wenhao Liu, Takumi Obana and Masataka Sata
Int. J. Mol. Sci. 2021, 22(21), 12081; https://doi.org/10.3390/ijms222112081 - 8 Nov 2021
Cited by 23 | Viewed by 4066
Abstract
Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has become a global pandemic with a great impact on social and economic activities, as well as public health. In most patients, the symptoms of COVID-19 are a high-grade fever [...] Read more.
Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has become a global pandemic with a great impact on social and economic activities, as well as public health. In most patients, the symptoms of COVID-19 are a high-grade fever and a dry cough, and spontaneously resolve within ten days. However, in severe cases, COVID-19 leads to atypical bilateral interstitial pneumonia, acute respiratory distress syndrome, and systemic thromboembolism, resulting in multiple organ failure with high mortality and morbidity. SARS-CoV-2 has immune evasion mechanisms, including inhibition of interferon signaling and suppression of T cell and B cell responses. SARS-CoV-2 infection directly and indirectly causes dysregulated immune responses, platelet hyperactivation, and endothelial dysfunction, which interact with each other and are exacerbated by cardiovascular risk factors. In this review, we summarize current knowledge on the pathogenic basis of thromboinflammation and endothelial injury in COVID-19. We highlight the distinct contributions of dysregulated immune responses, platelet hyperactivation, and endothelial dysfunction to the pathogenesis of COVID-19. In addition, we discuss potential therapeutic strategies targeting these mechanisms. Full article
(This article belongs to the Special Issue Cardiovascular Injuries in Severe Respiratory Infectious Diseases 2.0)
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