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Related Concept Videos

Inflammation01:38

Inflammation

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Myocarditis I: Introduction01:21

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Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...
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Myocarditis II: Clinical Features and Diagnostic Tests01:27

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Myocarditis is an inflammation of the heart muscle. The symptoms vary widely, encompassing asymptomatic presentations to severe, acute manifestations.Clinical PresentationAsymptomatic cases: In some instances, myocarditis may be asymptomatic, with the infection resolving without intervention. These cases often go undetected unless discovered incidentally through diagnostic imaging or tests conducted for other reasons.General Early Symptoms: Early symptoms of myocarditis are non-specific and can...
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Inflammatory Response I: Vascular and Cellular01:30

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The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
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Myocarditis III: Medical Management01:14

Myocarditis III: Medical Management

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Myocarditis: Comprehensive Medical ManagementMyocarditis, the heart muscle inflammation, requires a comprehensive medical management strategy that addresses the underlying cause, provides supportive care, manages symptoms, and reduces cardiac workload.Infections and Autoimmune CausesAdminister appropriate antimicrobial therapy when an infectious agent causes myocarditis. For instance, penicillin treats infections caused by Group A Streptococcus. In cases where autoimmune processes are...
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Inflammatory Response01:28

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An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
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Related Experiment Video

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In vivo Imaging Method to Distinguish Acute and Chronic Inflammation
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Metainflammation in COVID-19.

Mojtaba Bakhtiari1, Kamyar Asadipooya2

  • 1Toxicology and Cancer Biology Center, University of Kentucky, Lexington, KY, USA.

Endocrine, Metabolic & Immune Disorders Drug Targets
|January 5, 2022
PubMed
Summary
This summary is machine-generated.

Obesity increases COVID-19 severity by raising soluble ACE2 levels, aiding viral entry. Treatments targeting ACE2, TMPRSS2, and DPP4 show promise, with DPP4 inhibitors and spironolactone/eplerenone offering potential benefits.

Keywords:
ACE2COVID-19DPP4 inhibitorMetainflammationobesityspironolactone

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Area of Science:

  • Virology
  • Immunology
  • Metabolic Diseases

Background:

  • The COVID-19 pandemic, caused by SARS-CoV-2, poses a significant threat, particularly to vulnerable populations like the elderly, men, and those with comorbidities such as obesity.
  • Obesity is linked to metainflammation, potentially exacerbating COVID-19 severity through mechanisms involving the angiotensin-converting enzyme 2 (ACE2) pathway and immune dysregulation.

Purpose of the Study:

  • To explore the pathophysiological links between obesity, metainflammation, and COVID-19.
  • To investigate the role of ACE2, DPP4, and TMPRSS2 in SARS-CoV-2 entry and pathogenesis.
  • To identify potential therapeutic strategies targeting these pathways to improve COVID-19 outcomes.

Main Methods:

  • Review of existing literature on SARS-CoV-2, ACE2, DPP4, TMPRSS2, and obesity-related pathophysiology.
  • Analysis of the interaction between SARS-CoV-2 S-glycoprotein and host cell receptors (ACE2, DPP4).
  • Evaluation of the role of host proteases like TMPRSS2 in viral entry.

Main Results:

  • Increased soluble ACE2 levels in obesity may enhance SARS-CoV-2 entry, while membrane-bound ACE2 might offer protection against cytokine storms.
  • SARS-CoV-2 utilizes ACE2 and potentially DPP4 receptors for cell entry, with TMPRSS2 facilitating the process.
  • Several existing medications (metformin, statins, Orlistat, thiazolidinediones) show potential benefits, but a combination of DPP4 inhibitors and spironolactone/eplerenone appears most effective.

Conclusions:

  • Therapeutic strategies aimed at reducing soluble ACE2, antagonizing TMPRSS2, or blocking DPP4 could improve COVID-19 outcomes.
  • The combination of DPP4 inhibitors and spironolactone/eplerenone demonstrates a promising multi-targeted approach by reducing viral entry and mitigating inflammation.