Kakio T, Matsumori A
Department of Cardiovascular Medicine, Kyoto University.
Nihon Rinsho. 1997 Jun;55(6):1498-504.
The pathogenesis of viral myocarditis has not been clarified yet especially in the subacute and chronic stages. Recent reports have shown that myocarditis may be caused by autoimmune reactions. Autoantigens and autoantibodies have recently been reported in myocarditis and cardiomyopathy, and most of them may be induced by the cross-reaction between virus and cardiac tissue, molecular mimicry, or by the destruction of immune tolerance. However it is not clear how autoimmune reactions affect viral myocarditis. We have reported that cytokines are increased in the blood of patients with myocarditis and cardiomyopathy. Many kinds of cytokines modulate viral myocarditis in different ways in murine models. Nitric oxide is also recognized as an important factor in viral myocarditis. We have reported that drugs for heart failure modulate cytokine production. Classifying drugs from this point of view may be helpful for developing new therapeutic strategy for patients with myocarditis and cardiomyopathy.
病毒性心肌炎的发病机制尚未明确,尤其是在亚急性期和慢性期。最近的报告表明,心肌炎可能由自身免疫反应引起。自身抗原和自身抗体最近在心肌炎和心肌病中被报道,其中大多数可能是由病毒与心脏组织之间的交叉反应、分子模拟或免疫耐受的破坏所诱导。然而,尚不清楚自身免疫反应如何影响病毒性心肌炎。我们已经报道,心肌炎和心肌病患者血液中的细胞因子会增加。在小鼠模型中,多种细胞因子以不同方式调节病毒性心肌炎。一氧化氮也被认为是病毒性心肌炎中的一个重要因素。我们已经报道,用于治疗心力衰竭的药物可调节细胞因子的产生。从这一角度对药物进行分类可能有助于为心肌炎和心肌病患者制定新的治疗策略。