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1.
PLoS One ; 17(3): e0264178, 2022.
Article in English | MEDLINE | ID: covidwho-1731596

ABSTRACT

Renalase is a secreted flavoprotein with anti-inflammatory and pro-cell survival properties. COVID-19 is associated with disordered inflammation and apoptosis. We hypothesized that blood renalase levels would correspond to severe COVID-19 and survival. In this retrospective cohort study, clinicopathologic data and blood samples were collected from hospitalized COVID-19 subjects (March-June 2020) at a single institution tertiary hospital. Plasma renalase and cytokine levels were measured and clinical data abstracted from health records. Of 3,450 COVID-19 patients, 458 patients were enrolled. Patients were excluded if <18 years, or opted out of research. The primary composite outcome was intubation or death within 180 days. Secondary outcomes included mortality alone, intensive care unit admission, use of vasopressors, and CPR. Enrolled patients had mean age 64 years (SD±17), were 53% males, and 48% non-whites. Mean renalase levels was 14,108·4 ng/ml (SD±8,137 ng/ml). Compared to patients with high renalase, those with low renalase (< 8,922 ng/ml) were more likely to present with hypoxia, increased ICU admission (54% vs. 33%, p < 0.001), and cardiopulmonary resuscitation (10% vs. 4%, p = 0·023). In Cox proportional hazard model, every 1000 ng/ml increase in renalase decreased the risk of death or intubation by 5% (HR 0·95; 95% CI 0·91-0·98) and increased survival alone by 6% (HR 0·95; CI 0·90-0·98), after adjusting for socio-demographics, initial disease severity, comorbidities and inflammation. Patients with high renalase-low IL-6 levels had the best survival compared to other groups (p = 0·04). Renalase was independently associated with reduced intubation and mortality in hospitalized COVID-19 patients. Future studies should assess the pathophysiological relevance of renalase in COVID-19 disease.


Subject(s)
COVID-19/pathology , Monoamine Oxidase/blood , Adult , Aged , COVID-19/mortality , COVID-19/virology , Endothelium/metabolism , Endothelium/pathology , Female , Hospitalization , Humans , Intensive Care Units , Interleukin-6/blood , Kaplan-Meier Estimate , Male , Middle Aged , Proportional Hazards Models , Respiration, Artificial , Retrospective Studies , Risk Factors , SARS-CoV-2/isolation & purification , Severity of Illness Index
2.
Molecules ; 27(5)2022 Mar 01.
Article in English | MEDLINE | ID: covidwho-1715569

ABSTRACT

COVID-19 is an endothelial disease. All the major comorbidities that increase the risk for severe SARS-CoV-2 infection and severe COVID-19 including old age, obesity, diabetes, hypertension, respiratory disease, compromised immune system, coronary artery disease or heart failure are associated with dysfunctional endothelium. Genetics and environmental factors (epigenetics) are major risk factors for endothelial dysfunction. Individuals with metabolic syndrome are at increased risk for severe SARS-CoV-2 infection and poor COVID-19 outcomes and higher risk of mortality. Old age is a non-modifiable risk factor. All other risk factors are modifiable. This review also identifies dietary risk factors for endothelial dysfunction. Potential dietary preventions that address endothelial dysfunction and its sequelae may have an important role in preventing SARS-CoV-2 infection severity and are key factors for future research to address. This review presents some dietary bioactives with demonstrated efficacy against dysfunctional endothelial cells. This review also covers dietary bioactives with efficacy against SARS-CoV-2 infection. Dietary bioactive compounds that prevent endothelial dysfunction and its sequelae, especially in the gastrointestinal tract, will result in more effective prevention of SARS-CoV-2 variant infection severity and are key factors for future food research to address.


Subject(s)
Endothelium/drug effects , Flavonoids/pharmacology , Functional Food/analysis , SARS-CoV-2/drug effects , COVID-19/drug therapy , COVID-19/pathology , COVID-19/virology , Endothelium/metabolism , Flavonoids/metabolism , Flavonoids/therapeutic use , Humans , Polysaccharides/pharmacology , Polysaccharides/therapeutic use , Risk Factors , SARS-CoV-2/isolation & purification , Stilbenes/pharmacology , Stilbenes/therapeutic use , Terpenes/pharmacology , Terpenes/therapeutic use
3.
Int J Mol Sci ; 22(24)2021 Dec 17.
Article in English | MEDLINE | ID: covidwho-1580692

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 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.


Subject(s)
COVID-19/complications , Heart Failure/metabolism , Heart/virology , Animals , Blood/virology , Blood Physiological Phenomena/immunology , COVID-19/physiopathology , Cardiomegaly/metabolism , Cardiovascular Diseases/metabolism , Cardiovascular Physiological Phenomena/immunology , Disease Models, Animal , Endothelium/metabolism , Heart/physiopathology , Heart Failure/virology , Hydroxychloroquine/pharmacology , Male , Matrix Metalloproteinase 9/drug effects , Matrix Metalloproteinase 9/metabolism , Mice , Mice, Inbred C57BL , Muscle Cells/metabolism , Myocardium/metabolism , SARS-CoV-2/metabolism , SARS-CoV-2/pathogenicity , Ventricular Remodeling/physiology
4.
Front Immunol ; 12: 778913, 2021.
Article in English | MEDLINE | ID: covidwho-1574246

ABSTRACT

The current global pandemic of the Severe Acute Respiratory Syndrome CoronaVirus 2 (SARS-CoV-2) causing COVID-19, has infected millions of people and continues to pose a threat to many more. Angiotensin-Converting Enzyme 2 (ACE2) is an important player of the Renin-Angiotensin System (RAS) expressed on the surface of the lung, heart, kidney, neurons, and endothelial cells, which mediates SARS-CoV-2 entry into the host cells. The cytokine storms of COVID-19 arise from the large recruitment of immune cells because of the dis-synchronized hyperactive immune system, lead to many abnormalities including hyper-inflammation, endotheliopathy, and hypercoagulability that produce multi-organ dysfunction and increased the risk of arterial and venous thrombosis resulting in more severe illness and mortality. We discuss the aberrated interconnectedness and forthcoming crosstalks between immunity, the endothelium, and coagulation, as well as how sex disparities affect the severity and outcome of COVID-19 and harm men especially. Further, our conceptual framework may help to explain why persistent symptoms, such as reduced physical fitness and fatigue during long COVID, may be rooted in the clotting system.


Subject(s)
COVID-19/epidemiology , COVID-19/virology , SARS-CoV-2 , Biomarkers , Blood Coagulation , Blood Coagulation Disorders/diagnosis , Blood Coagulation Disorders/etiology , COVID-19/complications , COVID-19/diagnosis , Cytokines/metabolism , Disease Susceptibility , Endothelium/metabolism , Female , Host-Pathogen Interactions/immunology , Humans , Inflammation Mediators , Male , Renin-Angiotensin System , Severity of Illness Index , Sex Factors
5.
Mol Med ; 27(1): 151, 2021 12 03.
Article in English | MEDLINE | ID: covidwho-1551198

ABSTRACT

BACKGROUND: We investigated the feasibility of two biomarkers of endothelial damage (Syndecan-1 and thrombomodulin) in coronavirus disease 2019 (COVID-19), and their association with inflammation, coagulopathy, and mortality. METHODS: The records of 49 COVID-19 patients who were admitted to an intensive care unit (ICU) in Wuhan, China between February and April 2020 were examined. Demographic, clinical, and laboratory data, and outcomes were compared between survivors and non-survivors COVID-19 patients, and between patients with high and low serum Syndecan-1 levels. The dynamics of serum Syndecan-1 levels were also analyzed. RESULTS: The levels of Syndecan-1 were significantly higher in non-survivor group compared with survivor group (median 1031.4 versus 504.0 ng/mL, P = 0.002), and the levels of thrombomodulin were not significantly different between these two groups (median 4534.0 versus 3780.0 ng/mL, P = 0.070). Kaplan-Meier survival analysis showed that the group with high Syndecan-1 levels had worse overall survival (log-rank test: P = 0.023). Patients with high Syndecan-1 levels also had significantly higher levels of thrombomodulin, interleukin-6, and tumor necrosis factor-α. Data on the dynamics of Syndecan-1 levels indicated much greater variations in non-survivors than survivors. CONCLUSIONS: COVID-19 patients with high levels of Syndecan-1 develop more serious endothelial damage and inflammatory reactions, and have increased mortality. Syndecan-1 has potential for use as a marker for progression or severity of COVID-19. Protecting the glycocalyx from destruction is a potential treatment for COVID-19.


Subject(s)
COVID-19/blood , COVID-19/therapy , Endothelium/metabolism , Glycocalyx/metabolism , Syndecan-1/blood , Aged , Biomarkers/blood , Blood Coagulation , COVID-19/mortality , China/epidemiology , Cytokines/metabolism , Endothelium, Vascular/pathology , Female , Humans , Inflammation , Intensive Care Units , Interleukin-6/blood , Kaplan-Meier Estimate , Male , Middle Aged , Oxygen , ROC Curve , SARS-CoV-2 , Thrombomodulin/blood , Treatment Outcome , Tumor Necrosis Factor-alpha/blood
6.
Int J Mol Sci ; 22(21)2021 Nov 06.
Article in English | MEDLINE | ID: covidwho-1502441

ABSTRACT

On 11 March 2020, the World Health Organization (WHO) declared a pandemic due to the spread of COVID-19 from Wuhan, China, causing high mortality rates all over the world. The related disease, which mainly affects the lungs, is responsible for the onset of Diffuse Alveolar Damage (DAD) and a hypercoagulability state, frequently leading to Severe Acute Respiratory Syndrome (SARS) and multiorgan failure, particularly in old and severe-critically ill patients. In order to find effective therapeutic strategies, many efforts have been made aiming to shed light on the pathophysiology of COVID-19 disease. Moreover, following the late advent of vaccination campaigns, the need for the comprehension of the pathophysiology of the fatal, although rare, thrombotic adverse events has become mandatory as well. The achievement of such purposes needs a multidisciplinary approach, depending on a correct interpretation of clinical, biochemical, biomolecular, and forensic findings. In this scenario, autopsies have helped in defining, on both gross and histologic examinations, the main changes to which the affected organs undergo and the role in assessing whether a patient is dead "from" or "with" COVID-19, not to mention whether the existence of a causal link exists between vaccination and thrombotic adverse events. In the present work, we explored the role of postmortem immunohistochemistry, and the increasingly used ancillary technique, in helping to understand the mechanism underlying the pathophysiology of both COVID-19 disease and COVID-19 vaccine-related adverse and rare effects.


Subject(s)
COVID-19 Vaccines/adverse effects , COVID-19/pathology , Thrombosis/etiology , Autopsy , COVID-19/prevention & control , COVID-19/virology , COVID-19 Vaccines/administration & dosage , Cytokines/metabolism , Endothelium/metabolism , Endothelium/pathology , Humans , Immunohistochemistry , SARS-CoV-2/isolation & purification
7.
J Gen Virol ; 102(8)2021 08.
Article in English | MEDLINE | ID: covidwho-1369239

ABSTRACT

Viruses may exploit the cardiovascular system to facilitate transmission or within-host dissemination, and the symptoms of many viral diseases stem at least in part from a loss of vascular integrity. The microvascular architecture is comprised of an endothelial cell barrier ensheathed by perivascular cells (pericytes). Pericytes are antigen-presenting cells (APCs) and play crucial roles in angiogenesis and the maintenance of microvascular integrity through complex reciprocal contact-mediated and paracrine crosstalk with endothelial cells. We here review the emerging ways that viruses interact with pericytes and pay consideration to how these interactions influence microvascular function and viral pathogenesis. Major outcomes of virus-pericyte interactions include vascular leakage or haemorrhage, organ tropism facilitated by barrier disruption, including viral penetration of the blood-brain barrier and placenta, as well as inflammatory, neurological, cognitive and developmental sequelae. The underlying pathogenic mechanisms may include direct infection of pericytes, pericyte modulation by secreted viral gene products and/or the dysregulation of paracrine signalling from or to pericytes. Viruses we cover include the herpesvirus human cytomegalovirus (HCMV, Human betaherpesvirus 5), the retrovirus human immunodeficiency virus (HIV; causative agent of acquired immunodeficiency syndrome, AIDS, and HIV-associated neurocognitive disorder, HAND), the flaviviruses dengue virus (DENV), Japanese encephalitis virus (JEV) and Zika virus (ZIKV), and the coronavirus severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2; causative agent of coronavirus disease 2019, COVID-19). We touch on promising pericyte-focussed therapies for treating the diseases caused by these important human pathogens, many of which are emerging viruses or are causing new or long-standing global pandemics.


Subject(s)
Cell Physiological Phenomena , Disease Susceptibility , Host-Pathogen Interactions , Pericytes/virology , Virus Diseases/metabolism , Virus Diseases/virology , Animals , Cell Communication , Dengue Virus/physiology , Disease Management , Endothelial Cells/virology , Endothelium/metabolism , Endothelium/virology , HIV/physiology , Humans , Paracrine Communication , SARS-CoV-2/physiology , Virus Diseases/diagnosis , Virus Diseases/therapy , Virus Physiological Phenomena
9.
Viruses ; 13(1)2020 12 26.
Article in English | MEDLINE | ID: covidwho-1079698

ABSTRACT

The ongoing pandemic of coronavirus disease 2019 (COVID-19) caused by the acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) poses a persistent threat to global public health. Although primarily a respiratory illness, extrapulmonary manifestations of COVID-19 include gastrointestinal, cardiovascular, renal and neurological diseases. Recent studies suggest that dysfunction of the endothelium during COVID-19 may exacerbate these deleterious events by inciting inflammatory and microvascular thrombotic processes. Although controversial, there is evidence that SARS-CoV-2 may infect endothelial cells by binding to the angiotensin-converting enzyme 2 (ACE2) cellular receptor using the viral Spike protein. In this review, we explore current insights into the relationship between SARS-CoV-2 infection, endothelial dysfunction due to ACE2 downregulation, and deleterious pulmonary and extra-pulmonary immunothrombotic complications in severe COVID-19. We also discuss preclinical and clinical development of therapeutic agents targeting SARS-CoV-2-mediated endothelial dysfunction. Finally, we present evidence of SARS-CoV-2 replication in primary human lung and cardiac microvascular endothelial cells. Accordingly, in striving to understand the parameters that lead to severe disease in COVID-19 patients, it is important to consider how direct infection of endothelial cells by SARS-CoV-2 may contribute to this process.


Subject(s)
COVID-19/metabolism , Endothelial Cells/metabolism , Endothelium/metabolism , SARS-CoV-2/immunology , ADAM17 Protein/metabolism , Angiotensin-Converting Enzyme 2/metabolism , Antiviral Agents/therapeutic use , COVID-19/immunology , Coronavirus , Coronavirus Infections/metabolism , Endothelial Cells/immunology , Endothelium/immunology , Endothelium/virology , Endothelium, Vascular/immunology , Endothelium, Vascular/metabolism , Humans , Lung/metabolism , Thrombosis , Virus Replication
10.
Viruses ; 13(2)2021 01 22.
Article in English | MEDLINE | ID: covidwho-1045367

ABSTRACT

Respiratory viruses such as influenza and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are a constant threat to public health given their ability to cause global pandemics. Infection with either virus may lead to aberrant host responses, such as excessive immune cell recruitment and activation, dysregulated inflammation, and coagulopathy. These may contribute to the development of lung edema and respiratory failure. An increasing amount of evidence suggests that lung endothelial cells play a critical role in the pathogenesis of both viruses. In this review, we discuss how infection with influenza or SARS-CoV-2 may induce endothelial dysfunction. We compare the effects of infection of these two viruses, how they may contribute to pathogenesis, and discuss the implications for potential treatment. Understanding the differences between the effects of these two viruses on lung endothelial cells will provide important insight to guide the development of therapeutics.


Subject(s)
Endothelium/virology , Influenzavirus A/pathogenicity , Lung Injury/pathology , Lung Injury/virology , SARS-CoV-2/pathogenicity , Blood Platelets/metabolism , Cytokines/metabolism , Endothelial Cells/metabolism , Endothelial Cells/pathology , Endothelium/metabolism , Endothelium/pathology , Extracellular Traps/immunology , Humans , Intercellular Junctions/pathology , Lung Injury/therapy
11.
Biochemistry (Mosc) ; 85(12): 1543-1553, 2020 Dec.
Article in English | MEDLINE | ID: covidwho-1035276

ABSTRACT

Pathogenesis of the novel coronavirus infection COVID-19 is the subject of active research around the world. COVID-19 caused by the SARS-CoV-2 is a complex disease in which interaction of the virus with target cells, action of the immune system and the body's systemic response to these events are closely intertwined. Many respiratory viral infections, including COVID-19, cause death of the infected cells, activation of innate immune response, and secretion of inflammatory cytokines. All these processes are associated with the development of oxidative stress, which makes an important contribution to pathogenesis of the viral infections. This review analyzes information on the oxidative stress associated with the infections caused by SARS-CoV-2 and other respiratory viruses. The review also focuses on involvement of the vascular endothelium in the COVID-19 pathogenesis.


Subject(s)
COVID-19/pathology , Oxidative Stress , Angiotensin II/metabolism , Antioxidants/therapeutic use , COVID-19/drug therapy , COVID-19/virology , Cytokines/metabolism , Endothelium/cytology , Endothelium/metabolism , Humans , Immunity, Innate , Reactive Oxygen Species/metabolism , SARS-CoV-2/isolation & purification
12.
Cell Mol Life Sci ; 77(22): 4725-4727, 2020 Nov.
Article in English | MEDLINE | ID: covidwho-749426

ABSTRACT

P53 is a tumor suppressor protein, associated with strong anti-inflammatory activities. Recent evidence suggest that this transcription factor counteracts lung inflammatory diseases, including the lethal acute respiratory distress syndrome. Herein we provide a brief discussion on the relevant topic.


Subject(s)
Respiratory Distress Syndrome/metabolism , Tumor Suppressor Protein p53/metabolism , Cytokines/metabolism , Endothelium/metabolism , Humans , Inflammation/metabolism , Lung/metabolism , Permeability
13.
Emerg Top Life Sci ; 4(4): 379-387, 2020 12 11.
Article in English | MEDLINE | ID: covidwho-927716

ABSTRACT

There has not been any means to inhibit replication of the SARS-CoV-2 virus responsible for the rapid, deadly spread of the COVID-19 pandemic and an effective, safe, tested across diverse populations vaccine still requires extensive investigation. This review deals with the repurpose of a wellness technology initially fabricated for combating physical inactivity by increasing muscular activity. Its action increases pulsatile shear stress (PSS) to the endothelium such that the bioavailability of nitric oxide (NO) and other mediators are increased throughout the body. In vitro evidence indicates that NO inhibits SARS-CoV-2 virus replication but there are no publications of NO delivery to the virus in vivo. It will be shown that increased PSS has potential in vivo to exert anti-viral properties of NO as well as to benefit endothelial manifestations of COVID-19 thereby serving as a safe and effective backstop.


Subject(s)
COVID-19/therapy , Endothelium/metabolism , Nitric Oxide/metabolism , Physical Stimulation , Accelerometry , COVID-19/physiopathology , Exercise , Humans , Physical Stimulation/methods , Stress, Mechanical
14.
Am J Respir Cell Mol Biol ; 64(4): 407-415, 2021 04.
Article in English | MEDLINE | ID: covidwho-922610

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a new strain of a Coronaviridae virus that presents 79% genetic similarity to the severe acute respiratory syndrome coronavirus, has been recently recognized as the cause of a global pandemic by the World Health Organization, implying a major threat to world public health. SARS-CoV-2 infects host human cells by binding through the viral spike proteins to the ACE-2 (angiotensin-converting enzyme 2) receptor, fuses with the cell membrane, enters, and starts its replication process to multiply its viral load. Coronavirus disease (COVID-19) was initially considered a respiratory infection that could cause pneumonia. However, in severe cases, it extends beyond the respiratory system and becomes a multiorgan disease. This transition from localized respiratory infection to multiorgan disease is due to two main complications of COVID-19. On the one hand, it is due to the so-called cytokine storm: an uncontrolled inflammatory reaction of the immune system in which defensive molecules become aggressive for the body itself. On the other hand, it is due to the formation of a large number of thrombi that can cause myocardial infarction, stroke, and pulmonary embolism. The pulmonary endothelium actively participates in these two processes, becoming the last barrier before the virus spreads throughout the body. In this review, we examine the role of the pulmonary endothelium in response to COVID-19, the existence of potential biomarkers, and the development of novel therapies to restore vascular homeostasis and to protect and/or treat coagulation, thrombosis patients. In addition, we review the thrombotic complications recently observed in patients with COVID-19 and its potential threatening sequelae.


Subject(s)
COVID-19/metabolism , Endothelium/metabolism , Pulmonary Embolism/metabolism , SARS-CoV-2/metabolism , Thrombosis/metabolism , Angiotensin-Converting Enzyme 2/metabolism , Biomarkers/metabolism , COVID-19/pathology , COVID-19/therapy , Endothelium/pathology , Endothelium/virology , Humans , Membrane Fusion , Pulmonary Embolism/pathology , Pulmonary Embolism/therapy , Pulmonary Embolism/virology , Spike Glycoprotein, Coronavirus/metabolism , Thrombosis/pathology , Thrombosis/therapy , Thrombosis/virology
15.
Int J Dermatol ; 60(1): 73-80, 2021 Jan.
Article in English | MEDLINE | ID: covidwho-919217

ABSTRACT

BACKGROUND: Coronavirus disease 2019 (COVID-19) is a systemic multi-organ viral illness. Previous studies have found that many patients had a procoagulant state and/or severe hypoxemia with relatively well-preserved lung mechanics. Mechanisms underlying the damage to vascular tissues are not well-elucidated yet. Histological data in COVID-19 patients are still limited and are mainly focused on post-mortem analysis. Given that the skin is affected by COVID-19 and the relative ease of its histological examination, we aimed to examine the histology of skin lesions in COVID-19 patients to better understand the disease's pathology. METHODS: Five skin lesions from COVID-19 adult patients were selected for a deep histological tissue examination. RESULTS: A strong vasculopathic reaction pattern based on prominent vascular endothelial and myointimal cell growth was identified. Endothelial cell distortion generated vascular lumen obliteration and striking erythrocyte and serum extravasation. Significant deposition of C4d and C3 throughout the vascular cell wall was also identified. A regenerative epidermal hyperplasia with tissue structure preservation was also observed. CONCLUSIONS: COVID-19 could comprise an obliterative microangiopathy consisting on endothelial and myointimal growth with complement activation. This mechanism, together with the increased vascular permeability identified, could contribute to obliteration of the vascular lumen and hemorrhage in COVID-19. Thus, anticoagulation by itself could not completely reverse vascular lumen obliteration, with consequent increased risk of hemorrhage. Findings of this study could contribute to a better understanding of physiopathological mechanisms underlying COVID-19 on living patients and could help further studies find potential targets for specific therapeutic interventions in severe cases.


Subject(s)
COVID-19/complications , Endothelial Cells/pathology , Myocytes, Smooth Muscle/pathology , Skin Diseases/pathology , Vascular Diseases/pathology , Aged , Blood Vessels/pathology , CD3 Complex/metabolism , CD4 Antigens/metabolism , Endothelium/metabolism , Endothelium/pathology , Humans , Hyperplasia/pathology , Hyperplasia/virology , SARS-CoV-2 , Skin/blood supply , Skin Diseases/virology , Vascular Diseases/virology
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