scholarly journals Health concerns regarding the effect of the COVID-19 pandemic on male fertility

2021 ◽  
Author(s):  
Hamidreza Mosleh ◽  
Fatemeh Moradi ◽  
Mehdi Mehdizadeh ◽  
Marziyeh Ajdary ◽  
Alaa Moeinzadeh ◽  
...  
Keyword(s):  
Male Infertility ◽  
Sertoli Cells ◽  
Leydig Cells ◽  
Renin Angiotensin System ◽  
High Expression ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
Testicular Cells ◽  
Novel Coronavirus ◽  
High Expression Level

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel coronavirus found in China in 2019. The disease caused by SARS-CoV-2, coronavirus disease 2019 (COVID-19), has been found to be closely related to the cells that secrete angiotensin-converting enzyme 2 (ACE2). ACE2 is involved in the renin-angiotensin system and is widely secreted in several tissues, including the testis, which has raised concerns because organs with high expression of the ACE2 receptor are susceptible to infection. Analyses have shown that in testicular cells, such as spermatogonia, seminiferous duct cells, Sertoli cells, and Leydig cells, there is a high expression level of ACE2. Therefore, SARS-CoV-2 may damage male reproductive tissues and cause infertility. Since male infertility is an important problem, scientists are evaluating whether COVID-19 may influence male infertility through the ACE2 receptor.

scholarly journals Pathological Role of Angiotensin II in Severe COVID-19

TH Open ◽  
2020 ◽  
Vol 04 (02) ◽  
pp. e138-e144 ◽  
Author(s):  
Wolfgang Miesbach
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Treatment Options ◽  
Renin Angiotensin System ◽  
Target Cells ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
Renin Angiotensin ◽  
Novel Coronavirus

AbstractThe activated renin–angiotensin system induces a prothrombotic state resulting from the imbalance between coagulation and fibrinolysis. Angiotensin II is the central effector molecule of the activated renin–angiotensin system and is degraded by the angiotensin-converting enzyme 2 to angiotensin (1–7). The novel coronavirus infection (classified as COVID-19) is caused by the new coronavirus SARS-CoV-2 and is characterized by an exaggerated inflammatory response that can lead to severe manifestations such as acute respiratory distress syndrome, sepsis, and death in a proportion of patients, mostly elderly patients with preexisting comorbidities. SARS-CoV-2 uses the angiotensin-converting enzyme 2 receptor to enter the target cells, resulting in activation of the renin–angiotensin system. After downregulating the angiotensin-converting enzyme 2, the vasoconstrictor angiotensin II is increasingly produced and its counterregulating molecules angiotensin (1–7) reduced. Angiotensin II increases thrombin formation and impairs fibrinolysis. Elevated levels were strongly associated with viral load and lung injury in patients with severe COVID-19. Therefore, the complex clinical picture of patients with severe complications of COVID-19 is triggered by the various effects of highly expressed angiotensin II on vasculopathy, coagulopathy, and inflammation. Future treatment options should focus on blocking the thrombogenic and inflammatory properties of angiotensin II in COVID-19 patients.

scholarly journals Moderate Intensity Aerobic Exercise Potential Favorable Effect Against COVID-19: The Role of Renin-Angiotensin System and Immunomodulatory Effects

2021 ◽  
Vol 12 ◽  
Author(s):  
Hamid Arazi ◽  
Akram Falahati ◽  
Katsuhiko Suzuki
Keyword(s):  
Physical Exercise ◽  
Experimental Studies ◽  
Renin Angiotensin System ◽  
Potential Effect ◽  
Moderate Intensity ◽  
Favorable Effect ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
Renin Angiotensin ◽  
Novel Coronavirus

The coronavirus disease (COVID-19) pandemic is caused by a novel coronavirus (CoV) named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). As the angiotensin converting enzyme 2 (ACE2) is the cellular receptor of SARS-CoV-2, it has a strong interaction with the renin angiotensin system (RAS). Experimental studies have shown that the higher levels of ACE2 or increasing ACE2/ACE1 ratio improve COVID-19 outcomes through lowering inflammation and death. Aerobic moderate intensity physical exercise fights off infections by two mechanisms, the inhibition of ACE/Ang II/AT1-R pathway and the stimulation of ACE2/Ang-(1–7)/MasR axis. Exercise can also activate the anti-inflammatory response so that it can be a potential therapeutic strategy against COVID-19. Here, we summarize and focus the relation among COVID-19, RAS, and immune system and describe the potential effect of aerobic moderate intensity physical exercise against CoV as a useful complementary tool for providing immune protection against SARS-CoV-2 virus infection, which is a novel intervention that requires further investigation.

ACE2 as a potential target for management of novel coronavirus (nCoV- 2019)

2020 ◽  
Vol 17 ◽  
Author(s):  
Elham Foroozanfar ◽  
Mohamad Forouzanfar ◽  
Tahereh Farkhondeh ◽  
Saeed Samarghandian ◽  
Fatemeh Forouzanfar
Keyword(s):  
Specific Treatment ◽  
Renin Angiotensin System ◽  
Review Article ◽  
The Other ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
The World ◽  
Novel Coronavirus

Abstract:: A novel coronavirus termed nCoV-2019 caused an epidemic of acute respiratory syndrome in humans was first detected in Wuhan, China, in December 2019. nCoV-2019 resulted in thousands of cases of lethal disease all around the world. Unfortunately, there is no specific treatment yet so better understanding of the pathobiology of the disease can be helpful. The renin–angiotensin system and their products has several important physiological actions, On the other hand, this system involved in the pathogenesis of various diseases. In this context, this review article will briefly insights for understanding the role of angiotensin-converting enzyme 2 (ACE2) receptor as a potential attractive target for nCoV-2019- induced acute respiratory syndrome.

scholarly journals NF-κB-repressed Sirt3 mediates testicular cholesterol metabolism and cytoskeleton assembly via P450scc/SOD2 deacetylation during spermatogenesis

2021 ◽  
Author(s):  
Mei Wang ◽  
Ling Zeng ◽  
Yao Xiong ◽  
Xiao-fei Wang ◽  
Lin Cheng ◽  
...  
Keyword(s):  
Male Infertility ◽  
Germ Cells ◽  
Sertoli Cells ◽  
Male Fertility ◽  
Leydig Cells ◽  
Nuclear Translocation ◽  
Cholesterol Metabolism ◽  
Male Subfertility ◽  
Upstream Regulator ◽  
Testicular Cells

AbstractTesticular homeostasis requires the balanced interplay between specific molecules in Sertoli cells, Leydig cells, germ cells. Loss of this coordination can lead to the disruption of spermatogenesis, even male infertility. By operating the upregulation and downregulation of Sirt3 in our male subfertility rats model and two testicular cells models, we indicated that Sirt3 overexpression and activator ameliorated cholesterol metabolism via P450scc deacetylation in Leydig cells, and cytoskeleton assembly via PDLIM1 with SOD2 deacetylation in Sertoli cells and elongating spermatids. In terms of the upstream regulator of Sirt3, the phosphorylation of NF-κB p65Ser536 stimulated the nuclear translocation of NF-κB subunits (p50, p65, RelB), which bound to TFBS1 and TFBS2 synchronously in the promoter of Sirt3, repressing Sirt3 transcription. This study demonstrates that NF-κB-repressed SIRT3 acts directly on cholesterol metabolism of Leydig cells and cytoskeleton assembly of Sertoli cells via P450scc/SOD2 deacetylation to regulate sperm differentiation, influencing spermatogenesis, even male fertility.Research organism: Rat, mouse

scholarly journals Outcomes of COVID-19 Hospitalized Patients Previously Treated with Renin-Angiotensin System Inhibitors

2020 ◽  
Vol 9 (11) ◽  
pp. 3472 ◽  
Author(s):  
Elena-Mihaela Cordeanu ◽  
Lucas Jambert ◽  
Francois Severac ◽  
Hélène Lambach ◽  
Jonathan Tousch ◽  
...  
Keyword(s):  
Renin Angiotensin System ◽  
Severe Pneumonia ◽  
University Hospital ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
Renin Angiotensin ◽  
Previously Treated ◽  
The Impact ◽  
Harmful Effects ◽  
Observation Period

(1) Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) penetrates respiratory epithelium through angiotensin-converting enzyme-2 binding, raising concerns about the potentially harmful effects of renin–angiotensin system inhibitors (RASi) on Human Coronavirus Disease 2019 (COVID-19) evolution. This study aimed to provide insight into the impact of RASi on SARS-CoV-2 outcomes in patients hospitalized for COVID-19. (2) Methods: This was a retrospective analysis of hospitalized adult patients with SARS-CoV-2 infection admitted to a university hospital in France. The observation period ended at hospital discharge. (3) Results: During the study period, 943 COVID-19 patients were admitted to our institution, of whom 772 were included in this analysis. Among them, 431 (55.8%) had previously known hypertension. The median age was 68 (56–79) years. Overall, 220 (28.5%) patients were placed under mechanical ventilation and 173 (22.4%) died. According to previous exposure to RASi, we defined two groups, namely, “RASi” (n = 282) and “RASi-free” (n = 490). Severe pneumonia (defined as leading to death and/or requiring intubation, high-flow nasal oxygen, noninvasive ventilation, and/or oxygen flow at a rate of ≥5 L/min) and death occurred more frequently in RASi-treated patients (64% versus 53% and 29% versus 19%, respectively). However, in a propensity score-matched cohort derived from the overall population, neither death (hazard ratio (HR) 0.93 (95% confidence interval (CI) 0.57–1.50), p = 0.76) nor severe pneumonia (HR 1.03 (95%CI 0.73–1.44), p = 0.85) were associated with RASi therapy. (4) Conclusion: Our study showed no correlation between previous RASi treatment and death or severe COVID-19 pneumonia after adjustment for confounders.

scholarly journals ACE2: the molecular doorway to SARS-CoV-2

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Miriam Marlene Medina-Enríquez ◽  
Sandra Lopez-León ◽  
José Alberto Carlos-Escalante ◽  
Zuleika Aponte-Torres ◽  
Angelica Cuapio ◽  
...  
Keyword(s):  
Renin Angiotensin System ◽  
Cell Types ◽  
Negative Regulator ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
Functional Activities ◽  
Pathological Conditions ◽  
Organ Systems ◽  
Different Cell Types ◽  
Functional Receptor

AbstractThe angiotensin-converting enzyme 2 (ACE2) is the host functional receptor for the new virus SARS-CoV-2 causing Coronavirus Disease 2019. ACE2 is expressed in 72 different cell types. Some factors that can affect the expression of the ACE2 are: sex, environment, comorbidities, medications (e.g. anti-hypertensives) and its interaction with other genes of the renin-angiotensin system and other pathways. Different factors can affect the risk of infection of SARS-CoV-2 and determine the severity of the symptoms. The ACE2 enzyme is a negative regulator of RAS expressed in various organ systems. It is with immunity, inflammation, increased coagulopathy, and cardiovascular disease. In this review, we describe the genetic and molecular functions of the ACE2 receptor and its relation with the physiological and pathological conditions to better understand how this receptor is involved in the pathogenesis of COVID-19. In addition, it reviews the different comorbidities that interact with SARS-CoV-2 in which also ACE2 plays an important role. It also describes the different factors that interact with the virus that have an influence in the expression and functional activities of the receptor. The goal is to provide the reader with an understanding of the complexity and importance of this receptor.

scholarly journals ACE2 Shedding and the Role in COVID-19

2022 ◽  
Vol 11 ◽  
Author(s):  
Jieqiong Wang ◽  
Huiying Zhao ◽  
Youzhong An
Keyword(s):  
Amino Acids ◽  
Viral Entry ◽  
Kidney Injury ◽  
Renin Angiotensin System ◽  
Underlying Mechanism ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
Transmembrane Glycoprotein

Angiotensin converting enzyme 2 (ACE2), a transmembrane glycoprotein, is an important part of the renin-angiotensin system (RAS). In the COVID-19 epidemic, it was found to be the receptor of severe acute respiratory syndrome coronavirus 2 (SARS-COV-2). ACE2 maintains homeostasis by inhibiting the Ang II-AT1R axis and activating the Ang I (1-7)-MasR axis, protecting against lung, heart and kidney injury. In addition, ACE2 helps transport amino acids across the membrane. ACE2 sheds from the membrane, producing soluble ACE2 (sACE2). Previous studies have pointed out that sACE2 plays a role in the pathology of the disease, but the underlying mechanism is not yet clear. Recent studies have confirmed that sACE2 can also act as the receptor of SARS-COV-2, mediating viral entry into the cell and then spreading to the infective area. Elevated concentrations of sACE2 are more related to disease. Recombinant human ACE2, an exogenous soluble ACE2, can be used to supplement endogenous ACE2. It may represent a potent COVID-19 treatment in the future. However, the specific administration concentration needs to be further investigated.

scholarly journals Mechanism of ligand recognition by human ACE2 receptor

2020 ◽  
Author(s):  
Apurba Bhattarai ◽  
Shristi Pawnikar ◽  
Yinglong Miao
Keyword(s):  
Ligand Binding ◽  
Renin Angiotensin System ◽  
Rational Drug Design ◽  
Renal Diseases ◽  
Ligand Recognition ◽  
Conformational Ensemble ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
Accelerated Molecular Dynamics ◽  
Rational Drug

AbstractAngiotensin converting enzyme 2 (ACE2) plays a key role in renin-angiotensin system regulation and amino acid homeostasis. Human ACE2 acts as the receptor for severe acute respiratory syndrome coronaviruses SARS-CoV and SARS-CoV-2. ACE2 is also widely expressed in epithelial cells of lungs, heart, kidney and pancreas. It is considered an important drug target for treating SARS-CoV-2, as well as pulmonary diseases, heart failure, hypertension, renal diseases and diabetes. Despite the critical importance, the mechanism of ligand binding to the human ACE2 receptor remains unknown. Here, we address this challenge through all-atom simulations using a novel ligand Gaussian accelerated molecular dynamics (LiGaMD) method. Microsecond LiGaMD simulations have successfully captured both binding and unbinding of the MLN-4760 inhibitor in the ACE2 receptor. In the ligand unbound state, the ACE2 receptor samples distinct Open, Partially Open and Closed conformations. Ligand binding biases the receptor conformational ensemble towards the Closed state. The LiGaMD simulations thus suggest a conformational selection mechanism for ligand recognition by the ACE2 receptor. Our simulation findings are expected to facilitate rational drug design of ACE2 against coronaviruses and other related human diseases.

scholarly journals CLINICAL FEATURES OF NOVEL CORONAVIRUS 2019-INFECTED CASES WITH PRE-EXISTING CARDIOVASCULAR DISEASE, DISAGGREGATED BY GENDER

2021 ◽  
Vol 54 (2) ◽  
pp. 180-185
Author(s):  
Elham Mohammadyari ◽  
Mohammad Reza Kaffashian ◽  
Iraj Ahmadi ◽  
Azra Kenarkoohi ◽  
Askar Soufinia ◽  
...  
Keyword(s):  
Clinical Features ◽  
Clinical Laboratory ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Men And Women ◽  
Blood Pressures ◽  
Males And Females ◽  
The Mean ◽  
Novel Coronavirus ◽  
Common Laboratory

Objectives: This study was conducted to evaluate the clinical features of 68 coronavirus 2019-infected cardiac cases on gender basis. Methodology: Clinical, laboratory and electrocardiographic data of 68 COVID-19 patients with pre-existing cardiovascular diseases, analyzed and compared by gender-wise. Results: Dry cough (78% of male, 80% females) and fever (62% of male, 75% females) were the most common symptoms. Out of these 97% of them needed O2 supplementation. O2 saturation in patients with O2 therapy was 85%; 31% of men and 11% of women experienced intubation. The most common laboratory abnormalities, were neutrophilia, leukocytosis, lymphopenia, thrombocytopenia, decreased hemoglobin level, increased creatinine and urea, in men and women. Troponin level was different between male and female. Pneumonia was found in 86-87% patients. Approximately, Males and female, respectively53.10 and 52.8%, shown sinus tachycardia (ST arrythmia). PVC arrythmia was found in 2.9% of total patients. BBB arrythmia was found in 31.20% of males vs. 11.10% of females. The mean systole/diastole blood pressures respectively were 130±4/79.7 ±2 in males and 134±4/81±3 in females. Heart axis changes was identified in 43.8% and 27.8% of males and females respectively. Conclusion: Severity of symptoms and outcomes of COVID-19 in cardiac patients showed some differences between men and women which could be associated with differences in immune responses, respiratory tract properties, renin angiotensin system, sex hormones and lifestyle.  However, more studies to categorize gender differences are required.

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