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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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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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Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
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Cardiomyopathy IV: Restrictive Cardiomyopathy01:29

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Restrictive cardiomyopathy (RCM) is a rare heart muscle disease characterized by impaired ventricular filling due to stiffened ventricular walls, leading to significant diastolic dysfunction.EtiologyRestrictive cardiomyopathy can arise from both inherited and acquired diseases, many of which are systemic. It is categorized into four main types: infiltrative, storage, non-infiltrative, and endomyocardial diseases.Infiltrative diseases, such as amyloidosis, lead to RCM by depositing amyloid...
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Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
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Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.EtiologyVarious factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin,...
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ROS-Mediated Necroptosis Promotes Coxsackievirus B3 Replication and Myocardial Injury.

Junbo Huang1, Yanjun Di1, Qing Song1

  • 1School of Medicine, Huaqiao University, Quanzhou 362021, China.

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|October 29, 2025
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Coxsackievirus B3 (CVB3) triggers necroptosis, a form of cell death, by increasing reactive oxygen species (ROS) and inhibiting the Nrf2/HO-1 pathway. This finding offers new therapeutic targets for viral myocarditis.

Keywords:
RIP1RIP3ROScoxsackievirus B3necroptosisviral myocarditis

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Area of Science:

  • Cardiology
  • Virology
  • Molecular Biology

Background:

  • Coxsackievirus B3 (CVB3) causes viral myocarditis (VMC), leading to heart failure.
  • The role of CVB3 in inducing necroptosis remains unclear.

Purpose of the Study:

  • Investigate CVB3-induced necroptosis mechanisms.
  • Determine the effect of necroptosis on viral replication.

Main Methods:

  • Utilized in vitro (HeLa cells) and in vivo (mouse models) to study CVB3 infection.
  • Measured necroptotic markers (RIP1, RIP3), reactive oxygen species (ROS), and Nrf2/HO-1 pathway activity.
  • Administered necroptosis inhibitor (Necrostatin-1) and ROS scavenger (N-acetylcysteine).

Main Results:

  • CVB3 infection upregulated RIP1 and RIP3, increased ROS, and suppressed the Nrf2/HO-1 pathway.
  • Necrostatin-1 and N-acetylcysteine treatment reduced cell death, viral replication, and myocardial injury.
  • CVB3 inhibits Nrf2/HO-1, causing ROS accumulation and promoting necroptosis.

Conclusions:

  • CVB3 induces ROS-dependent necroptosis via Nrf2/HO-1 pathway suppression.
  • This mechanism contributes to viral myocarditis pathogenesis.
  • Targeting this pathway offers potential therapeutic strategies for VMC.