ACE inhibitor suppresses cardiac remodeling after myocardial infarction by regulating dendritic cells and AT2 receptor-mediated mechanism in mice - 17/05/19
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Graphical abstract |
Highlights |
• | Cardioprotective effects of ACEI were enhanced through attenuating DCs migration via AT2R. |
• | DCs immune inflammatory response is repressed via down-regulating DCs maturation surface markers and inflammatory cytokines by AT2R. |
• | The role of AT2R in the process of DCs regulation via ACEI could provide new therapeutic insight for post-MI therapy. |
Abstract |
Dendritic cells (DCs) play a complex role in the progression of myocardial infarction (MI). The impact of angiotensin-converting enzyme (ACE) inhibitor therapy, partly via affecting DCs maturation and recruitment, was tested on a MI mouse model. Furthermore, the cardioprotective effects of ACEI were enhanced through attenuating migration of DCs from the spleen into peripheral circulation, thereby inhibiting DCs maturation and tissue inflammation. ACEI repress DCs immune inflammatory response through down-regulating DCs maturation surface markers and regulating inflammatory cytokines, which led to a higher survival rate, improved function and remodeling through decreased inflammatory response after MI. However, inhibition of AT2R activation, resulted in a reduction of ACEI effects on DCs. The potent anti-inflammatory effect of ACEI can partially be attributed to its impact on DCs through activation of AT2R, which may provide a new target mechanism for ACEI therapy after MI.
Le texte complet de cet article est disponible en PDF.Keywords : Dendritic cell, ACE inhibitor, Myocardial infarction, AT2 receptor, Inflammation
Plan
Vol 114
Article 108660- juin 2019 Retour au numéro
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