Immune mediators in inflammatory heart disease: Insights from a mouse model

M. Afanasyeva, N. R. Rose

Research output: Contribution to journalArticle

Abstract

Cardiac myosin-induced murine myocarditis provides a useful model for assessing the role of immune mediators in the development of inflammatory heart disease. Myocarditis is characterized by leucocyte infiltration, fibrosis, and cardiomyocyte death, which collectively lead to deterioration of both systolic and diastolic function as assessed by pressure-volume relations. In severe cases, disease progresses to dilated cardiomyopathy and heart failure. Key factors that promote disease include complement, tumour necrosis factor-alpha, interleukin-4, and interleukin-12. Factors found to suppress myocarditis include interferon-gamma, interleukin-10, and cyotoxic T lymphocyte antigen-4. Final disease outcome is determined by the interplay of these immune mediators.

Original languageEnglish (US)
JournalEuropean Heart Journal, Supplement
Volume4
Issue numberI
DOIs
StatePublished - Dec 2002

Fingerprint

Myocarditis
Heart Diseases
Cardiac Myosins
Viral Tumor Antigens
Dilated Cardiomyopathy
Interleukin-12
Cardiac Myocytes
Interleukin-4
Interleukin-10
Interferon-gamma
Leukocytes
Fibrosis
Heart Failure
Tumor Necrosis Factor-alpha
T-Lymphocytes
Pressure

Keywords

  • Autoimmunity
  • Cardiomyopathy
  • Cytokines
  • Knockout mice
  • Myocarditis
  • Pressure-volume relations

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Immune mediators in inflammatory heart disease : Insights from a mouse model. / Afanasyeva, M.; Rose, N. R.

In: European Heart Journal, Supplement, Vol. 4, No. I, 12.2002.

Research output: Contribution to journalArticle

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