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<p>Myocardial apoptosis is a cardinal process in acute viral myocarditis (VMC) instigated by coxsackievirus B3 (CVB3) infection. The anti-apoptotic regulator protein deglycase DJ-1 (DJ-1) is implicated in several pathological processes, yet its role in CVB3-induced VMC remains obscure. In this study, we decipher the protective role of DJ-1 against VMC. We found decreased DJ-1 expression in CVB3-infected H9C2 cells and VMC mouse heart tissues. DJ-1 knockout exacerbated VMC severity and apoptosis. Conversely, recovery of DJ-1 levels showed protective effects in vitro and in vivo. We observed downregulation of Dusp1 in DJ-1-deficient mice hearts and H9C2 cells with DJ-1 silencing. Subsequent in vitro assays corroborated that downregulation of DJ-1 amplifies apoptosis in H9C2 cells following CVB3 infection. This effect is mediated through the suppression of Dusp1 expression, thereby triggering the activation of the P38MAPK signaling pathway. Overall, our findings underscore DJ-1 as an appealing therapeutic target for VMC, with its anti-apoptotic effects in CVB3-induced VMC mediated in part via the Dusp1/P38MAPK signaling pathway. This novel understanding of DJ-1’s regulation might provide fresh insights into the pathogenesis of VMC and a potential therapeutic avenue for VMC.</p><p></p>

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Protein deglycase DJ-1 deficiency aggravates acute viral myocarditis by promoting apoptosis via reducing Dusp1 expression

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月28日

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  • Pengcheng Yan,
  • Shuai Feng,
  • Baona Li,
  • Wenchao Yin,
  • Leiyan Wang,
  • Gang Zhao,
  • Mengqi Guo,
  • Zhaoyang Wang,
  • Haitao Yuan

摘要

Myocardial apoptosis is a cardinal process in acute viral myocarditis (VMC) instigated by coxsackievirus B3 (CVB3) infection. The anti-apoptotic regulator protein deglycase DJ-1 (DJ-1) is implicated in several pathological processes, yet its role in CVB3-induced VMC remains obscure. In this study, we decipher the protective role of DJ-1 against VMC. We found decreased DJ-1 expression in CVB3-infected H9C2 cells and VMC mouse heart tissues. DJ-1 knockout exacerbated VMC severity and apoptosis. Conversely, recovery of DJ-1 levels showed protective effects in vitro and in vivo. We observed downregulation of Dusp1 in DJ-1-deficient mice hearts and H9C2 cells with DJ-1 silencing. Subsequent in vitro assays corroborated that downregulation of DJ-1 amplifies apoptosis in H9C2 cells following CVB3 infection. This effect is mediated through the suppression of Dusp1 expression, thereby triggering the activation of the P38MAPK signaling pathway. Overall, our findings underscore DJ-1 as an appealing therapeutic target for VMC, with its anti-apoptotic effects in CVB3-induced VMC mediated in part via the Dusp1/P38MAPK signaling pathway. This novel understanding of DJ-1’s regulation might provide fresh insights into the pathogenesis of VMC and a potential therapeutic avenue for VMC.