scholarly journals Damage to the cardiovascular system in COVID-19

2021 ◽  
Vol 2021 (1) ◽  
pp. 10-16
Author(s):  
O.M. Korzh ◽  
Keyword(s):  
Cardiovascular System ◽  
Qt Interval ◽  
Cardiovascular Events ◽  
Viral Infections ◽  
Cardiovascular Complications ◽  
Daily Monitoring ◽  
Direct Invasion ◽  
Cardiovascular Side Effects ◽  
The Relationship

COVID-19 affects not only the respiratory system, but also the cardiovascular system. The damage to the cardiovascular system in COVID-19 is multifactorial and several mechanisms are involved, including direct invasion, inflammation, thrombosis, autoantibody synthesis, and oxygen imbalance. The inflammation causes the release of cytokines, especially interleukin-6, and damage to cardiomyocytes. The overproduction of cytokines leads to an abnormal inflammatory response called a cytokine storm, which is believed to be the culprit in cardiovascular events in COVID-19 patients. Treatment of COVID-19 patients with cardiovascular complications is mostly supportive. The role of pharmacological blocking of the renin-angiotensin-aldosterone system in patients with cardiovascular disease and COVID-19 infection requires further research as the relationship appears to be very complex. To date, professional cardiological societies do not recommend canceling ACE inhibitors or agiotensin II receptor antagonists for patients taking these drugs for other indications. Special care should be taken about the potential cardiovascular side effects of the various therapies used to treat viral infections. When using them, daily monitoring of the QT interval on the ECG is proposed.

scholarly journals Dengue Virus and the Relationship with MicroRNAs

2020 ◽  
Author(s):  
Samir Casseb ◽  
Karla de Melo
Keyword(s):  
Dengue Virus ◽  
Viral Infection ◽  
Viral Infections ◽  
Immune Defense ◽  
Tropical Regions ◽  
Denv Serotypes ◽  
History Of ◽  
Infection Processes ◽  
The Relationship

Dengue is an acute febrile disease caused by a virus of the genus Flavivirus, family Flaviviridae, endemic in tropical regions of the globe. The agent is a virus with single-stranded RNA, classified into four distinct dengue virus (DENV) serotypes: DENV-1, DENV-2, DENV-3, and DENV-4. The host’s innate and adaptive immune responses play an essential role in determining the natural history of viral infections, especially in dengue. In this context, it has observed in recent years that the presence of RNA interference (RNAi) in viral infection processes is increasing, as well as immune defense. The context microRNAs (miRNAs) go for stood out, as their presence during viral infection, both in the replication of the virus and in the defense against these infections, becomes increasingly noticeable, therefore, making it increasingly necessary to better understand the role of these small RNAs within viral infection by DENV and what their consequences are in aggravating the consequences of patients affected by this disease.

scholarly journals The Role of MSC Therapy in Attenuating the Damaging Effects of the Cytokine Storm Induced by COVID-19 on the Heart and Cardiovascular System

2020 ◽  
Vol 7 ◽  
Author(s):  
Georgina M. Ellison-Hughes ◽  
Liam Colley ◽  
Katie A. O'Brien ◽  
Kirsty A. Roberts ◽  
Thomas A. Agbaedeng ◽  
...  
Keyword(s):  
Cardiovascular System ◽  
Cardiovascular Complications ◽  
Multiple Organ ◽  
Cytokine Storm ◽  
Cell Therapies ◽  
Tissue Repair And Regeneration ◽  
Global Pandemic ◽  
Organ Systems

The global pandemic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that causes coronavirus disease 2019 (COVID-19) has led to 47 m infected cases and 1. 2 m (2.6%) deaths. A hallmark of more severe cases of SARS-CoV-2 in patients with acute respiratory distress syndrome (ARDS) appears to be a virally-induced over-activation or unregulated response of the immune system, termed a “cytokine storm,” featuring elevated levels of pro-inflammatory cytokines such as IL-2, IL-6, IL-7, IL-22, CXCL10, and TNFα. Whilst the lungs are the primary site of infection for SARS-CoV-2, in more severe cases its effects can be detected in multiple organ systems. Indeed, many COVID-19 positive patients develop cardiovascular complications, such as myocardial injury, myocarditis, cardiac arrhythmia, and thromboembolism, which are associated with higher mortality. Drug and cell therapies targeting immunosuppression have been suggested to help combat the cytokine storm. In particular, mesenchymal stromal cells (MSCs), owing to their powerful immunomodulatory ability, have shown promise in early clinical studies to avoid, prevent or attenuate the cytokine storm. In this review, we will discuss the mechanistic underpinnings of the cytokine storm on the cardiovascular system, and how MSCs potentially attenuate the damage caused by the cytokine storm induced by COVID-19. We will also address how MSC transplantation could alleviate the long-term complications seen in some COVID-19 patients, such as improving tissue repair and regeneration.

scholarly journals Protein O-GlcNAcylation: a new signaling paradigm for the cardiovascular system

2009 ◽  
Vol 296 (1) ◽  
pp. H13-H28 ◽  
Author(s):  
Boglarka Laczy ◽  
Bradford G. Hill ◽  
Kai Wang ◽  
Andrew J. Paterson ◽  
C. Roger White ◽  
...  
Keyword(s):  
Adverse Effects ◽  
Cardiovascular System ◽  
Protein Modification ◽  
Cell Function ◽  
Cardiovascular Function ◽  
Cardiovascular Complications ◽  
Protective Mechanisms ◽  
Cytoplasmic Proteins ◽  
Present Understanding

The posttranslational modification of serine and threonine residues of nuclear and cytoplasmic proteins by the O-linked attachment of the monosaccharide β- N-acetylglucosamine ( O-GlcNAc) is a highly dynamic and ubiquitous protein modification. Protein O-GlcNAcylation is rapidly emerging as a key regulator of critical biological processes including nuclear transport, translation and transcription, signal transduction, cytoskeletal reorganization, proteasomal degradation, and apoptosis. Increased levels of O-GlcNAc have been implicated as a pathogenic contributor to glucose toxicity and insulin resistance, which are both major hallmarks of diabetes mellitus and diabetes-related cardiovascular complications. Conversely, there is a growing body of data demonstrating that the acute activation of O-GlcNAc levels is an endogenous stress response designed to enhance cell survival. Reports on the effect of altered O-GlcNAc levels on the heart and cardiovascular system have been growing rapidly over the past few years and have implicated a role for O-GlcNAc in contributing to the adverse effects of diabetes on cardiovascular function as well as mediating the response to ischemic injury. Here, we summarize our present understanding of protein O-GlcNAcylation and its effect on the regulation of cardiovascular function. We examine the pathways regulating protein O-GlcNAcylation and discuss, in more detail, our understanding of the role of O-GlcNAc in both mediating the adverse effects of diabetes as well as its role in mediating cellular protective mechanisms in the cardiovascular system. In addition, we also explore the parallels between O-GlcNAc signaling and redox signaling, as an alternative paradigm for understanding the role of O-GlcNAcylation in regulating cell function.

Deleterious effects of viral pneumonia on cardiovascular system

2020 ◽  
Vol 41 (19) ◽  
pp. 1833-1838 ◽  
Author(s):  
Jiahao Duan ◽  
Yeshun Wu ◽  
Cunming Liu ◽  
Chun Yang ◽  
Ling Yang
Keyword(s):  
Viral Infection ◽  
Cardiovascular System ◽  
Cardiovascular Events ◽  
Causes Of Death ◽  
Viral Infections ◽  
Cardiovascular Response ◽  
Clinical Manifestations ◽  
Viral Pneumonia ◽  
Influenza Pandemics ◽  
Epidemiological Characteristics

Abstract Viral pneumonia has a significant effect on the cardiovascular system through various mechanisms; even though it is traditionally regarded as a pulmonary disease characterized by dyspnoea and hypoxaemia. Recent research works have shown that cardiovascular events outweigh all other causes of death in various influenza pandemics. Therefore, the exploration of the effects of viral pneumonia on cardiovascular system becomes increasingly essential. The objective of this review is three-fold: first, to summarize the knowledge about the epidemiological characteristics and clinical manifestations of viral infections that are the recent causes of global pandemics; second, to explore the cardiovascular response to these infections; and third, to attempt in identifying the possible coping strategies of the Wuhan epidemic and the future viral infection pandemics.

IL-6 induced enhanced clearance of proANP and ANP by insulin-degrading enzyme in T1DM mouse

2021 ◽  
Author(s):  
Caiyun Li ◽  
Yao Wang ◽  
Guozhen Zhu ◽  
Yaxian Shang ◽  
Kang Jiefang ◽  
...  
Keyword(s):  
Type I Diabetes ◽  
Cardiovascular Complications ◽  
Mapk Signaling ◽  
Type I ◽  
Insulin Degrading Enzyme ◽  
Cvd Risk ◽  
Degrading Enzyme ◽  
The Relationship ◽  
Dose Dependent Increase

Cardiovascular disease (CVD) is the prevalent cause of morbidity and mortality in type I diabetes mellitus (T1DM) worldwide. However, the pathophysiological mechanisms underlying the relationship between CVD, CVD risk factors, and T1DM have not yet been sufficiently explored. Here we reported that insulin-degrading enzyme (IDE) effectively degrades the precursor of atrial natriuretic peptide (proANP) intracellular in HEK293T cells. Pro-inflammatory cytokine IL-6 elicited a significant dose-dependent increase in IDE protein expression. Inhibition of ERK/MAPK signaling pathway with selumetinib abolished IL-6-stimulated increase in IDE protein level and deceased in ANP secretion in H9C2 cells. Importantly, the T1DM mouse model displayed lower proANP in the heart and ANP in serum, due to increased IDE expression and activity. Our outcomes suggest a novel role of IL-6 on ANP metabolism via IDE and provide the possibilities for new potential therapeutic strategies for diabetes-related cardiovascular complications.

scholarly journals The Relationship of the Mechanisms of the Pathogenesis of Multiple Sclerosis and the Expression of Endogenous Retroviruses

Biology ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 464
Author(s):  
Vera R. Lezhnyova ◽  
Ekaterina V. Martynova ◽  
Timur I. Khaiboullin ◽  
Richard A. Urbanowicz ◽  
Svetlana F. Khaiboullina ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Viral Infections ◽  
Endogenous Retroviruses ◽  
Epigenetic Mechanisms ◽  
Humoral Factors ◽  
Human Endogenous Retroviruses ◽  
Relationship Of ◽  
The Relationship

Two human endogenous retroviruses of the HERV-W family can act as cofactors triggering multiple sclerosis (MS): MS-associated retrovirus (MSRV) and ERVWE1. Endogenous retroviral elements are believed to have integrated in our ancestors’ DNA millions of years ago. Their involvement in the pathogenesis of various diseases, including neurodegenerative pathologies, has been demonstrated. Numerous studies have shown a correlation between the deterioration of patients’ health and increased expression of endogenous retroviruses. The exact causes and mechanisms of endogenous retroviruses activation remains unknown, which hampers development of therapeutics. In this review, we will summarize the main characteristics of human endogenous W retroviruses and describe the putative mechanisms of activation, including epigenetic mechanisms, humoral factors as well as the role of the exogenous viral infections.

scholarly journals Regulation of Chemokines and Cytokines by Histone Deacetylases and an Update on Histone Decetylase Inhibitors in Human Diseases

2019 ◽  
Vol 20 (5) ◽  
pp. 1110 ◽  
Author(s):  
Himavanth Gatla ◽  
Nethaji Muniraj ◽  
Prashanth Thevkar ◽  
Siddhartha Yavvari ◽  
Sahithi Sukhavasi ◽  
...  
Keyword(s):  
Histone Deacetylases ◽  
Viral Infections ◽  
Kidney Diseases ◽  
Hdac Inhibitors ◽  
Cardiovascular Complications ◽  
Human Diseases ◽  
Wide Range ◽  
Hematological Cancers ◽  
Anti Tumor Activity

Histone acetyltransferases (HATs) and histone deacetylases (HDACs) counteract with each other to regulate gene expression by altering chromatin structure. Aberrant HDAC activity was reported in many human diseases including wide range of cancers, viral infections, cardiovascular complications, auto-immune diseases and kidney diseases. HDAC inhibitors are small molecules designed to block the malignant activity of HDACs. Chemokines and cytokines control inflammation, immunological and other key biological processes and are shown to be involved in various malignancies. Various HDACs and HDAC inhibitors were reported to regulate chemokines and cytokines. Even though HDAC inhibitors have remarkable anti-tumor activity in hematological cancers, they are not effective in treating many diseases and many patients relapse after treatment. However, the role of HDACs and cytokines in regulating these diseases still remain unclear. Therefore, understanding exact mechanisms and effector functions of HDACs are urgently needed to selectively inhibit them and to establish better a platform to combat various malignancies. In this review, we address regulation of chemokines and cytokines by HDACs and HDAC inhibitors and update on HDAC inhibitors in human diseases.

scholarly journals Unraveling the Relationship of Asthma and COVID-19

2021 ◽  
Vol 11 (12) ◽  
pp. 1374
Author(s):  
Agamemnon Bakakos ◽  
Petros Bakakos ◽  
Nikoletta Rovina
Keyword(s):  
Molecular Mechanisms ◽  
Viral Infections ◽  
Asthma Severity ◽  
Current Evidence ◽  
Asthma Exacerbations ◽  
Inflammatory Phenotypes ◽  
Relationship Of ◽  
The Impact ◽  
The Relationship

Viral infections are one of the main causes of asthma exacerbations. During the COVID-19 era, concerns regarding the relationship of SARS-CoV2 with asthma have been raised. The concerns are both for COVID severity and asthma exacerbations. Many studies on COVID-19 epidemiology and comorbidities have assessed whether asthma represents a risk factor for SARS-CoV2 infection and/or more severe course of the disease. This review covers the current evidence on the prevalence of asthma in COVID-19 and its association with susceptibility to and severity of SARS-CoV2 infection. It will examine the possible role of underlying asthma severity in COVID-19 related outcomes as well as the molecular mechanisms involved in the co-existence of these entities. The possible role of asthma inflammatory phenotypes will also be evaluated. Finally, the impact of asthma comorbidities and the implications of asthma medication on COVID-19 will be addressed.

scholarly journals Gamma Delta T Cells and Their Involvement in COVID-19 Virus Infections

2021 ◽  
Vol 12 ◽  
Author(s):  
Georg von Massow ◽  
Steve Oh ◽  
Alan Lam ◽  
Kenth Gustafsson
Keyword(s):  
T Cells ◽  
Viral Infections ◽  
Cell Subset ◽  
Γδ T Cells ◽  
Common Symptom ◽  
Virus Infections ◽  
Infected Cells ◽  
The Relationship

The global outbreak of the SARS-Cov-2 virus in 2020 has killed millions of people worldwide and forced large parts of the world into lockdowns. While multiple vaccine programs are starting to immunize the global population, there is no direct cure for COVID-19, the disease caused by the SARS-Cov-2 infection. A common symptom in patients is a decrease in T cells, called lymphopenia. It is as of yet unclear what the exact role of T cells are in the immune response to COVID-19. The research so far has mainly focused on the involvement of classical αβ T cells. However, another subset of T cells called γδ T cells could have an important role to play. As part of the innate immune system, γδ T cells respond to inflammation and stressed or infected cells. The γδ T cell subset appears to be particularly affected by lymphopenia in COVID-19 patients and commonly express activation and exhaustion markers. Particularly in children, this subset of T cells seems to be most affected. This is interesting and relevant because γδ T cells are more prominent and active in early life. Their specific involvement in this group of patients could indicate a significant role for γδ T cells in this disease. Furthermore, they seem to be involved in other viral infections and were able to kill SARS infected cells in vitro. γδ T cells can take up, process and present antigens from microbes and human cells. As e.g. tumour-associated antigens are presented by MHC on γδ T cells to classical T-cells, we argue here that it stands to reason that also viral antigens, such as SARS-Cov-2-derived peptides, can be presented in the same way. γδ T cells are already used for medical purposes in oncology and have potential in cancer therapy. As γδ T cells are not necessarily able to distinguish between a transformed and a virally infected cell it could therefore be of great interest to investigate further the relationship between COVID-19 and γδ T cells.

scholarly journals The relationship between the combined use of various proton pump inhibitors with antiplatelet drugs and the risk of cardiovascular complications

2019 ◽  
Vol 91 (8) ◽  
pp. 118-126 ◽  
Author(s):  
O D Ostroumova ◽  
A I Kochetkov ◽  
A P Pereverzev ◽  
E V Kravchenko ◽  
A N Kazjulin ◽  
...  
Keyword(s):  
Cardiovascular Risk ◽  
Drug Interactions ◽  
Proton Pump Inhibitors ◽  
Proton Pump ◽  
Cardiovascular Events ◽  
Cardiovascular Complications ◽  
Inclusion Criteria ◽  
Combined Use ◽  
Meta Analyses ◽  
The Relationship

In the article the problem of the combined use of clopidogrel and various proton pump inhibitors (PPIs) in terms of cardiovascular complications risk and stent thrombosis is considered. The results of meta - analyses and a systematic reviews affecting this issue are represented in detail. The inter - drug interactions mechanisms of various PPIs with clopidogrel based on the characteristics of the metabolism in the liver cytochromes system are discussed. The authors conducted a search, systematization and analysis of studies regarding the association between cardiovascular risk and combined use of individual medications from PPI class with clopidogrel, and these results are presented in the review. Currently available data do not allow to answer the question about the differences between individual PPIs in their impact on the risk of adverse cardiovascular events due to the small number of such studies, design heterogeneity, differences in the inclusion criteria and end points as well as in the rate of administration of individual PPIs.

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