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Cardiovascular Injuries in Severe Respiratory Infectious Diseases
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Cardiovascular Injuries in Severe Respiratory Infectious 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 (31 March 2021) | Viewed by 33393

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 recent reports from the most front-line researchers and clinicians fighting against coronavirus disease 19 (COVID-19), substantial deaths of individuals infected by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may be, at least in part, explained by non-respiratory fatal conditions, such as cardiovascular-related complications. However, little is elucidated about mechanisms of cardiovascular injuries in several severe respiratory infectious diseases, including COVID-19 and SARS-CoV-2. 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 Special Issue highly welcomes mechanical, experimental, and translational studies widely addressing this topic. Importantly, this special issue is not limited to the COVID-19 and SARS-CoV-2. Article, Full Review and Communication are welcome to contribute to our special issue.

Dr. Atsushi Tanaka
Prof. Dr. Koichi Node
Guest Editors

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Keywords

  • Severe respiratory infectious diseases
  • Cardiovascular disease
  • COVID-19
  • SARS-CoV-2

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Published Papers (7 papers)

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Research

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19 pages, 3738 KiB  
Article
Tumor Necrosis Factor-Alpha Exacerbates Viral Entry in SARS-CoV2-Infected iPSC-Derived Cardiomyocytes
by Chiu-Yang Lee, Chih-Heng Huang, Elham Rastegari, Vimalan Rengganaten, Ping-Cheng Liu, Ping-Hsing Tsai, Yuan-Fan Chin, Jing-Rong Wu, Shih-Hwa Chiou, Yuan-Chi Teng, Chih-Wei Lee, Yanwen Liang, An-Yu Chen, Shu-Chen Hsu, Yi-Jen Hung, Jun-Ren Sun, Chian-Shiu Chien and Yueh Chien
Int. J. Mol. Sci. 2021, 22(18), 9869; https://doi.org/10.3390/ijms22189869 - 13 Sep 2021
Cited by 13 | Viewed by 3593
Abstract
The coronavirus disease 2019 (COVID-19) pandemic with high infectivity and mortality has caused severe social and economic impacts worldwide. Growing reports of COVID-19 patients with multi-organ damage indicated that severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) may also disturb the cardiovascular system. Herein, [...] Read more.
The coronavirus disease 2019 (COVID-19) pandemic with high infectivity and mortality has caused severe social and economic impacts worldwide. Growing reports of COVID-19 patients with multi-organ damage indicated that severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) may also disturb the cardiovascular system. Herein, we used human induced pluripotent stem cell (iPSC)-derived cardiomyocytes (iCMs) as the in vitro platform to examine the consequence of SARS-CoV2 infection on iCMs. Differentiated iCMs expressed the primary SARS-CoV2 receptor angiotensin-converting enzyme-II (ACE2) and the transmembrane protease serine type 2 (TMPRSS2) receptor suggesting the susceptibility of iCMs to SARS-CoV2. Following the infection of iCMs with SARS-CoV2, the viral nucleocapsid (N) protein was detected in the host cells, demonstrating the successful infection. Bioinformatics analysis revealed that the SARS-CoV2 infection upregulates several inflammation-related genes, including the proinflammatory cytokine tumor necrosis factor-α (TNF-α). The pretreatment of iCMs with TNF-α for 24 h, significantly increased the expression of ACE2 and TMPRSS2, SASR-CoV2 entry receptors. The TNF-α pretreatment enhanced the entry of GFP-expressing SARS-CoV2 pseudovirus into iCMs, and the neutralization of TNF-α ameliorated the TNF-α-enhanced viral entry. Collectively, SARS-CoV2 elevated TNF-α expression, which in turn enhanced the SARS-CoV2 viral entry. Our findings suggest that, TNF-α may participate in the cytokine storm and aggravate the myocardial damage in COVID-19 patients. Full article
(This article belongs to the Special Issue Cardiovascular Injuries in Severe Respiratory Infectious Diseases)
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13 pages, 33428 KiB  
Article
Molecular Mechanisms of Palmitic Acid Augmentation in COVID-19 Pathologies
by Christie Joshi, Viren Jadeja and Heping Zhou
Int. J. Mol. Sci. 2021, 22(13), 7127; https://doi.org/10.3390/ijms22137127 - 1 Jul 2021
Cited by 11 | Viewed by 3302
Abstract
The coronavirus disease 2019 (COVID-19) pandemic has claimed over 2.7 million lives globally. Obesity has been associated with increased severity and mortality of COVID-19. However, the molecular mechanisms by which obesity exacerbates COVID-19 pathologies are not well-defined. The levels of free fatty acids [...] Read more.
The coronavirus disease 2019 (COVID-19) pandemic has claimed over 2.7 million lives globally. Obesity has been associated with increased severity and mortality of COVID-19. However, the molecular mechanisms by which obesity exacerbates COVID-19 pathologies are not well-defined. The levels of free fatty acids (FFAs) are elevated in obese subjects. This study was therefore designed to examine how excess levels of different FFAs may affect the progression of COVID-19. Biological molecules associated with palmitic acid (PA) and COVID-19 were retrieved from QIAGEN Knowledge Base, and Ingenuity Pathway Analysis tools were used to analyze these datasets and explore the potential pathways affected by different FFAs. Our study found that one of the top 10 canonical pathways affected by PA was the coronavirus pathogenesis pathway, mediated by key inflammatory mediators, including PTGS2; cytokines, including IL1β and IL6; chemokines, including CCL2 and CCL5; transcription factors, including NFκB; translation regulators, including EEF1A1; and apoptotic mediators, including BAX. In contrast, n-3 fatty acids may attenuate PA’s activation of the coronavirus pathogenesis pathway by inhibiting the activity of such mediators as IL1β, CCL2, PTGS2, and BAX. Furthermore, PA may modulate the expression of ACE2, the main cell surface receptor for the SARS-CoV-2 spike protein. Full article
(This article belongs to the Special Issue Cardiovascular Injuries in Severe Respiratory Infectious Diseases)
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14 pages, 2863 KiB  
Article
Erythrocyte, Platelet, Serum Ferritin, and P-Selectin Pathophysiology Implicated in Severe Hypercoagulation and Vascular Complications in COVID-19
by Chantelle Venter, Johannes Andries Bezuidenhout, Gert Jacobus Laubscher, Petrus Johannes Lourens, Janami Steenkamp, Douglas B. Kell and Etheresia Pretorius
Int. J. Mol. Sci. 2020, 21(21), 8234; https://doi.org/10.3390/ijms21218234 - 3 Nov 2020
Cited by 64 | Viewed by 7109
Abstract
Progressive respiratory failure is seen as a major cause of death in severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2)-induced infection. Relatively little is known about the associated morphologic and molecular changes in the circulation of these patients. In particular, platelet and erythrocyte pathology [...] Read more.
Progressive respiratory failure is seen as a major cause of death in severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2)-induced infection. Relatively little is known about the associated morphologic and molecular changes in the circulation of these patients. In particular, platelet and erythrocyte pathology might result in severe vascular issues, and the manifestations may include thrombotic complications. These thrombotic pathologies may be both extrapulmonary and intrapulmonary and may be central to respiratory failure. Previously, we reported the presence of amyloid microclots in the circulation of patients with coronavirus disease 2019 (COVID-19). Here, we investigate the presence of related circulating biomarkers, including C-reactive protein (CRP), serum ferritin, and P-selectin. These biomarkers are well-known to interact with, and cause pathology to, platelets and erythrocytes. We also study the structure of platelets and erythrocytes using fluorescence microscopy (using the markers PAC-1 and CD62PE) and scanning electron microscopy. Thromboelastography and viscometry were also used to study coagulation parameters and plasma viscosity. We conclude that structural pathologies found in platelets and erythrocytes, together with spontaneously formed amyloid microclots, may be central to vascular changes observed during COVID-19 progression, including thrombotic microangiopathy, diffuse intravascular coagulation, and large-vessel thrombosis, as well as ground-glass opacities in the lungs. Consequently, this clinical snapshot of COVID-19 strongly suggests that it is also a true vascular disease and considering it as such should form an essential part of a clinical treatment regime. Full article
(This article belongs to the Special Issue Cardiovascular Injuries in Severe Respiratory Infectious Diseases)
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Review

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13 pages, 14647 KiB  
Review
Pathophysiological Association of Endothelial Dysfunction with Fatal Outcome in COVID-19
by Tatsuya Maruhashi and Yukihito Higashi
Int. J. Mol. Sci. 2021, 22(10), 5131; https://doi.org/10.3390/ijms22105131 - 12 May 2021
Cited by 31 | Viewed by 3632
Abstract
The outbreak of coronavirus disease 2019 (COVID-19) caused by the betacoronavirus SARS-CoV-2 is now a worldwide challenge for healthcare systems. Although the leading cause of mortality in patients with COVID-19 is hypoxic respiratory failure due to viral pneumonia and acute respiratory distress syndrome, [...] Read more.
The outbreak of coronavirus disease 2019 (COVID-19) caused by the betacoronavirus SARS-CoV-2 is now a worldwide challenge for healthcare systems. Although the leading cause of mortality in patients with COVID-19 is hypoxic respiratory failure due to viral pneumonia and acute respiratory distress syndrome, accumulating evidence has shown that the risk of thromboembolism is substantially high in patients with severe COVID-19 and that a thromboembolic event is another major complication contributing to the high morbidity and mortality in patients with COVID-19. Endothelial dysfunction is emerging as one of the main contributors to the pathogenesis of thromboembolic events in COVID-19. Endothelial dysfunction is usually referred to as reduced nitric oxide bioavailability. However, failures of the endothelium to control coagulation, inflammation, or permeability are also instances of endothelial dysfunction. Recent studies have indicated the possibility that SARS-CoV-2 can directly infect endothelial cells via the angiotensin-converting enzyme 2 pathway and that endothelial dysfunction caused by direct virus infection of endothelial cells may contribute to thrombotic complications and severe disease outcomes in patients with COVID-19. In this review, we summarize the current understanding of relationships between SARS-CoV-2 infection, endothelial dysfunction, and pulmonary and extrapulmonary complications in patients with COVID-19. Full article
(This article belongs to the Special Issue Cardiovascular Injuries in Severe Respiratory Infectious Diseases)
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12 pages, 605 KiB  
Review
Cardiovascular Outcomes in the Acute Phase of COVID-19
by Hiroki Nakano, Kazuki Shiina and Hirofumi Tomiyama
Int. J. Mol. Sci. 2021, 22(8), 4071; https://doi.org/10.3390/ijms22084071 - 15 Apr 2021
Cited by 12 | Viewed by 2469
Abstract
The cumulative number of cases in the current global coronavirus disease 19 (COVID-19) pandemic, caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has exceeded 100 million, with the number of deaths caused by the infection having exceeded 2.5 million. Recent [...] Read more.
The cumulative number of cases in the current global coronavirus disease 19 (COVID-19) pandemic, caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has exceeded 100 million, with the number of deaths caused by the infection having exceeded 2.5 million. Recent reports from most frontline researchers have revealed that SARS-CoV-2 can also cause fatal non-respiratory conditions, such as fatal cardiovascular events. One of the important mechanisms underlying the multiple organ damage that is now known to occur during the acute phase of SARS-CoV-2 infection is impairment of vascular function associated with inhibition of angiotensin-converting enzyme 2. To manage the risk of vascular dysfunction-related complications in patients with COVID-19, it would be pivotal to clearly elucidate the precise mechanisms by which SARS-CoV-2 infects endothelial cells to cause vascular dysfunction. In this review, we summarize the current state of knowledge about the mechanisms involved in the development of vascular dysfunction in the acute phase of COVID-19. Full article
(This article belongs to the Special Issue Cardiovascular Injuries in Severe Respiratory Infectious Diseases)
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22 pages, 9759 KiB  
Review
Vascular Endothelial Glycocalyx Damage in COVID-19
by Minako Yamaoka-Tojo
Int. J. Mol. Sci. 2020, 21(24), 9712; https://doi.org/10.3390/ijms21249712 - 19 Dec 2020
Cited by 67 | Viewed by 6030
Abstract
The new coronavirus disease-2019 (COVID-19), which is spreading around the world and threatening people, is easily infecting a large number of people through airborne droplets; moreover, patients with hypertension, diabetes, obesity, and cardiovascular disease are more likely to experience severe conditions. Vascular endothelial [...] Read more.
The new coronavirus disease-2019 (COVID-19), which is spreading around the world and threatening people, is easily infecting a large number of people through airborne droplets; moreover, patients with hypertension, diabetes, obesity, and cardiovascular disease are more likely to experience severe conditions. Vascular endothelial dysfunction has been suggested as a common feature of high-risk patients prone to severe COVID-19, and measurement of vascular endothelial function may be recommended for predicting severe conditions in high-risk patients with COVID-19. However, fragmented vascular endothelial glycocalyx (VEGLX) is elevated in COVID-19 patients, suggesting that it may be useful as a prognostic indicator. Although the relationship between VEGLX and severe acute respiratory syndrome coronavirus 2 infections has not been well studied, some investigations into COVID-19 have clarified the relationship between VEGLX and the mechanism that leads to severe conditions. Clarifying the usefulness of VEGLX assessment as a predictive indicator of the development of severe complications is important as a strategy for confronting pandemics caused by new viruses with a high affinity for the vascular endothelium that may recur in the future. Full article
(This article belongs to the Special Issue Cardiovascular Injuries in Severe Respiratory Infectious Diseases)
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21 pages, 1868 KiB  
Review
Emerging Mechanisms of Pulmonary Vasoconstriction in SARS-CoV-2-Induced Acute Respiratory Distress Syndrome (ARDS) and Potential Therapeutic Targets
by Harry Karmouty-Quintana, Rajarajan A. Thandavarayan, Steven P. Keller, Sandeep Sahay, Lavannya M. Pandit and Bindu Akkanti
Int. J. Mol. Sci. 2020, 21(21), 8081; https://doi.org/10.3390/ijms21218081 - 29 Oct 2020
Cited by 42 | Viewed by 6459
Abstract
The 1918 influenza killed approximately 50 million people in a few short years, and now, the world is facing another pandemic. In December 2019, a novel coronavirus named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused an international outbreak of a respiratory [...] Read more.
The 1918 influenza killed approximately 50 million people in a few short years, and now, the world is facing another pandemic. In December 2019, a novel coronavirus named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused an international outbreak of a respiratory illness termed coronavirus disease 2019 (COVID-19) and rapidly spread to cause the worst pandemic since 1918. Recent clinical reports highlight an atypical presentation of acute respiratory distress syndrome (ARDS) in COVID-19 patients characterized by severe hypoxemia, an imbalance of the renin–angiotensin system, an increase in thrombogenic processes, and a cytokine release storm. These processes not only exacerbate lung injury but can also promote pulmonary vascular remodeling and vasoconstriction, which are hallmarks of pulmonary hypertension (PH). PH is a complication of ARDS that has received little attention; thus, we hypothesize that PH in COVID-19-induced ARDS represents an important target for disease amelioration. The mechanisms that can promote PH following SARS-CoV-2 infection are described. In this review article, we outline emerging mechanisms of pulmonary vascular dysfunction and outline potential treatment options that have been clinically tested. Full article
(This article belongs to the Special Issue Cardiovascular Injuries in Severe Respiratory Infectious Diseases)
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