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Abstract：
Cardiac injury may have multiple causes, including ischaemic, non-ischaemic, autoimmune, and infectious triggers. Independent of the underlying pathophysiology, cardiac tissue damage induces an inflammatory response to initiate repair processes. Immune cells are recruited to the heart to remove dead cardiomyocytes, which is essential for cardiac healing. Insufficient clearance of dying cardiomyocytes after myocardial infarction (MI) has been shown to promote unfavourable cardiac remodelling, which may result in heart failure (HF). Although immune cells are integral key players of cardiac healing, an unbalanced or unresolved immune reaction aggravates tissue damage that triggers maladaptive remodelling and HF. Neutrophils and macrophages are involved in both, inflammatory as well as reparative processes. Stimulating the resolution of cardiac inflammation seems to be an attractive therapeutic strategy to prevent adverse remodelling. Along with numerous experimental studies, the promising outcomes from recent clinical trials testing canakinumab or colchicine in patients with MI are boosting the interest in novel therapies targeting inflammation in cardiovascular disease patients. The aim of this review is to discuss recent experimental studies that provide new insights into the signalling pathways and local regulators within the cardiac microenvironment promoting the resolution of inflammation and tissue regeneration. We will cover ischaemia- and non-ischaemic-induced as well as infection-related cardiac remodelling and address potential targets to prevent adverse cardiac remodelling.
摘要：
心脏损伤可能有多种原因,包括缺血,非缺血性，自身免疫，和传染性触发器。独立于潜在的病理生理学，心脏组织损伤诱导炎症反应以启动修复过程。免疫细胞被募集到心脏来去除死亡的心肌细胞，这对心脏愈合至关重要。心肌梗死（MI）后死亡的心肌细胞清除不足已被证明会促进不利的心脏重塑，这可能导致心力衰竭（HF）。尽管免疫细胞是心脏愈合不可或缺的关键角色，不平衡或未解决的免疫反应会加剧组织损伤，从而引发适应性不良重塑和HF。中性粒细胞和巨噬细胞都参与其中，炎症和修复过程。刺激心脏炎症的消退似乎是防止不良重塑的有吸引力的治疗策略。随着大量的实验研究，最近在MI患者中测试卡纳单抗或秋水仙碱的临床试验的有希望的结果是提高了人们对针对心血管疾病患者炎症的新疗法的兴趣.这篇综述的目的是讨论最近的实验研究，这些研究为促进炎症和组织再生的心脏微环境中的信号通路和局部调节因子提供了新的见解。我们将涵盖缺血性和非缺血性引起的以及与感染相关的心脏重塑，并解决潜在的目标，以防止不良心脏重塑。
