scholarly journals Prospective: Evolution of Chinese Medicine to Treat COVID-19 Patients in China

2021 ◽  
Vol 11 ◽  
Author(s):  
Jieya Wu ◽  
Baoguo Sun ◽  
Li Hou ◽  
Fulan Guan ◽  
Liyuan Wang ◽  
...  
Keyword(s):  
Chinese Medicine ◽  
Renin Angiotensin System ◽  
Chinese Government ◽  
The Novel ◽  
Angiotensin System ◽  
Medical Needs ◽  
Anti Inflammatory ◽  
Underlying Mechanisms ◽  
Novel Coronavirus ◽  
The Individual

During the outbreak of the novel coronavirus disease (COVID-19), the Chinese government took a series of public health measures to tackle the outbreak and recommended six traditional Chinese medicine (TCM) evolved formulas, collectively referred to as “3-drugs-3-formulas”, for the treatment. In this prospective article, we will discuss how these six formulas evolved from TCM and what their underlying mechanisms of actions may be by evaluating the historical usage of the component formulas, the potential targeted pathways for the individual herbs used by STAR (signal transduction activity response) database from our laboratory, and the pathogenesis of COVID-19. Five of the six recommended formulas are administered orally, while the sixth is taken as an injection. Five classic categories of herbs in the six formulas including “Qing-Re”, “Qu-Shi”, “Huo-Xue”, “Bu-Yi” and “Xing-Qi” herbs are used based on different stages of disease. All five oral formulas build upon the core formula Maxingshigan Decoction (MD) which has anti-inflammatory and perhaps antiviral actions. While MD can have some desired effects, it may not be sufficient to treat COVID-19 on its own; consequently, complementary classic formulas and/or herbs have been added to potentiate each recommended formula’s anti-inflammatory, and perhaps anti-renin-angiotensin system (RAS)-mediated bradykinin storm (RBS) and antiviral effects to address the unique medical needs for different stages of COVID-19. The key actions of these formulas are likely to control systemic inflammation and/or RBS. The usage of Chinese medicine in the six formulas is consistent with the pathogenesis of COVID-19. Thus, an integrative systems biology approach—combining botanical treatments of conventional antiviral, anti-inflammatory or anti-RBS drugs to treat COVID-19 and its complications – should be explored.

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 Placental Vacuolar ATPase Function Is a Key Link between Multiple Causes of Preeclampsia

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Dongxin Zhang ◽  
Duyun Ye ◽  
Hongxiang Chen
Keyword(s):  
Molecular Mechanisms ◽  
Renin Angiotensin System ◽  
Vacuolar Atpase ◽  
Therapeutic Interventions ◽  
The Novel ◽  
Lipoxin A4 ◽  
Angiotensin System ◽  
Dihydroxyvitamin D ◽  
System 1 ◽  
Multiple Causes

Preeclampsia, a relatively common pregnancy disorder, is one of the major causes of maternal and fetal morbidity and mortality. Despite numerous research, the etiology of this syndrome remains not well understood as the pathogenesis of preeclampsia is complex, involving interaction between genetic, immunologic, and environmental factors. Preeclampsia, originating in placenta abnormalities, is induced by the circulating factors derived from the abnormal placenta. Recent work has identified various molecular mechanisms related to placenta development, including renin-angiotensin system, 1, 25-dihydroxyvitamin D, and lipoxin A4. Interestingly, advances suggest that vacuolar ATPase, a key molecule in placentation, is closely associated with them. Therefore, this intriguing molecule may represent an important link between various causes of preeclampsia. Here, we review that vacuolar ATPase works as a key link between multiple causes of preeclampsia and discuss the potential molecular mechanisms. The novel findings outlined in this review may provide promising explanations for the causation of preeclampsia and a rationale for future therapeutic interventions for this condition.

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.

scholarly journals Impact of air pollution and smoking on COVID-19: a review

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Vijaytha Vijayakumar ◽  
A. Sabu ◽  
M. Haridas
Keyword(s):  
Air Pollution ◽  
Renin Angiotensin System ◽  
Main Body ◽  
Angiotensin System ◽  
Forested Areas ◽  
Clean Air ◽  
Severity Of The Disease ◽  
Earth Day ◽  
The Individual ◽  
Tract Infections

Abstract Background The 21st century already witnessed many deadly epidemics and pandemics. The major ones were respiratory tract infections like SARS (2003), H1N1 (2009), MERS (2012) and the most recent pandemic COVID-19 (2019). The COVID-19 story begins when pneumonia of unknown cause was reported in the WHO country office of China at the end of 2019. SARS-CoV-2 is the causative agent that enters the host through the receptor ACE2, a component of the renin–angiotensin system. Main body of the abstract Symptoms of COVID-19 varies from patient to patient. It is all about the immunity and health status of the individual that decides the severity of the disease. The review focuses on the significant and often prevailing factors, those that influence the lung function. The factors that compromise the lung functions which may prepare the ground for severe COVID-19 infection are interestingly looked into. Focus was more on air pollution and cigarette smoke. Short conclusion The fact that the forested areas across the world show very low COVID-19 infection rate suggests that we are in need of the “Clean Air” on the fiftieth anniversary of World Earth Day. As many policies are implemented worldwide to protect from SARS-CoV-2, one simple remedy that we forgot was clean air can save lives. SARS-CoV-2 infects our lungs, and air pollution makes us more susceptible. In this crucial situation, the focus is only on the main threat; all other conditions are only in words to console the situation.

scholarly journals The Renin Angiotensin System — Its Physiology and Role in Disease States

1983 ◽  
Vol 11 (4) ◽  
pp. 369-376 ◽  
Author(s):  
G. S. Stokes
Keyword(s):  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Disease States ◽  
Electrolyte Depletion ◽  
Predominant Factor ◽  
The Individual ◽  
Effective Use ◽  
Selection Of

The renin-angiotensin system is one of a number of interlinked mechanisms regulating vascular resistance and blood volume. Under certain conditions it may become a predominant factor in maintaining vascular tone. Knowledge about these conditions (sodium depletion, mineralocorticoid deficiency, renovascular hypertension and iatrogenic hyperreninaemic states) is important for the safe and effective use of drugs which inhibit the renin-angiotensin system. Measurements of plasma renin activity are useful in the diagnostic assessment of hypertensive patients with hypokalaemia or evidence of renal artery stenosis. They may also have a place in the management of refractory or dialysis-resistant hypertension. Their use in the selection of antihypertensive therapy for the individual patient is controversial. Sequential measurements of plasma renin are helpful in analysing states of electrolyte depletion, and in titrating therapy for Addison's disease.

Vitamin D Deficiency and Cardiovascular Diseases

2020 ◽  
Vol 12 (1) ◽  
pp. 27-37
Author(s):  
Yifei Wang ◽  
Shi Zhou ◽  
Shuai Lei ◽  
Liying Hao ◽  
Deri Sun ◽  
...  
Keyword(s):  
Vitamin D ◽  
Cardiovascular Diseases ◽  
Vitamin D Deficiency ◽  
Cardiovascular Events ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Hormone Effects ◽  
Peptide Expression ◽  
Novel Strategy ◽  
Underlying Mechanisms

In recent years, there are increasing evidences of epidemiology and clinic which indicate that vitamin D deficiency has relationship with cardiovascular disease. It was found the levels of vitamin D were negatively correlated with cardiovascular events such as hypertension, heart failure, atrial fibrillation and coronary heart disease. This article reviews the connection between cardiovascular diseases and vitamin D, and explains the underlying mechanisms including regulating renin-angiotensin system or endothelial function, inhibition of natriuretic peptide expression or the release of parathyroid hormone, effects on inflammation or obesity, bioenergetics, activation of extracellular Ca2+, inhibition of oxidative stress, and so on. These mechanisms provide novel strategy for the treatment of these cardiovascular diseases.

scholarly journals Alamandine: Potential Protective Effects in SARS-CoV-2 Patients

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Ava Soltani Hekmat ◽  
Kazem Javanmardi
Keyword(s):  
Pulmonary Fibrosis ◽  
Renin Angiotensin System ◽  
The Body ◽  
Host Cells ◽  
Protective Effects ◽  
Ang Ii ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
Anti Inflammatory ◽  
G Protein Coupled

Coronavirus disease 2019 (COVID-19) can occur due to contracting severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 has no confined treatment and, consequently, has high hospitalization and mortality rates. Moreover, people who contract COVID-19 present systemic inflammatory spillover. It is now known that COVID-19 pathogenesis is linked to the renin-angiotensin system (RAS). COVID-19 invades host cells via the angiotensin-converting enzyme 2 (ACE2) receptor—as such, an individual’s susceptibility to COVID-19 increases alongside the upregulation of this receptor. COVID-19 has also been associated with interstitial pulmonary fibrosis, which leads to acute respiratory distress, cardiomyopathy, and shock. These outcomes are thought to result from imbalances in angiotensin (Ang) II and Ang-(1-7)/alamandine activity. ACE2, Ang-(1-7), and alamandine have potent anti-inflammatory properties, and some SARS-CoV-2 patients exhibit high levels of ACE2 and Ang-(1-7). This phenomenon could indicate a failing physiological response to prevent or reduce the severity of inflammation-mediated pulmonary injuries. Alamandine, which is another protective component of the RAS, has several health benefits owing to its antithrombogenic, anti-inflammatory, and antifibrotic characteristics. Alamandine alleviates pulmonary fibrosis via the Mas-related G protein-coupled receptor D (MrgD). Thus, a better understanding of this pathway could uncover novel pharmacological strategies for altering proinflammatory environments within the body. Following such strategies could inhibit fibrosis after SARS-CoV-2 infection and, consequently, prevent COVID-19.

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