Why the study?
Dendritic cells play a complex role in the progression of MI, but the impact of ACE inhibitor therapy via dendritic cell maturation and recruitment was unclear.
Does ACE inhibitor therapy improve survival and cardiac remodeling in a myocardial infarction mouse model?
Does ACE inhibitor therapy improve survival and cardiac remodeling in a myocardial infarction mouse model?
ACE inhibitors suppress cardiac remodeling and improve survival after MI in mice by regulating dendritic cells via an AT2 receptor-mediated mechanism.
Does not support practice change; hypothesis-generating for AT2R-dendritic cell mechanisms in human MI.
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.
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Ma et al. (2019) studied this question.
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