PDF(Pubmed)
Abstract：
Myocardial infarction (MI) sets off a complex inflammatory cascade that is crucial for effective cardiac healing and scar formation. Yet, if this response becomes excessive or uncontrolled, it can lead to cardiovascular complications. This review aims to provide a comprehensive overview of the tightly regulated local inflammatory response triggered in the early post-MI phase involving cardiomyocytes, (myo)fibroblasts, endothelial cells, and infiltrating immune cells. Next, we explore how the bone marrow and extramedullary hematopoiesis (such as in the spleen) contribute to sustaining immune cell supply at a cardiac level. Lastly, we discuss recent findings on how metabolic cardiovascular risk factors, including hypercholesterolemia, hypertriglyceridemia, diabetes, and hypertension, disrupt this immunological response and explore the potential modulatory effects of lifestyle habits and pharmacological interventions. Understanding how different metabolic risk factors influence the inflammatory response triggered by MI and unraveling the underlying molecular and cellular mechanisms may pave the way for developing personalized therapeutic approaches based on the patient\'s metabolic profile. Similarly, delving deeper into the impact of lifestyle modifications on the inflammatory response post-MI is crucial. These insights may enable the adoption of more effective strategies to manage post-MI inflammation and improve cardiovascular health outcomes in a holistic manner.
摘要：
心肌梗塞（MI）引发了复杂的炎症级联反应，这对于有效的心脏愈合和疤痕形成至关重要。然而，如果这种反应变得过度或不受控制，会导致心血管并发症.这篇综述旨在全面概述在涉及心肌细胞的MI后早期阶段触发的紧密调节的局部炎症反应。（myo）成纤维细胞，内皮细胞，和浸润免疫细胞。接下来,我们探讨骨髓和髓外造血（如脾脏）如何有助于维持心脏水平的免疫细胞供应。最后,我们讨论了代谢心血管危险因素的最新发现，包括高胆固醇血症,高甘油三酯血症,糖尿病,和高血压，破坏这种免疫反应，探索生活习惯和药物干预的潜在调节作用。了解不同的代谢风险因素如何影响MI引发的炎症反应，并揭示潜在的分子和细胞机制，可能为开发基于患者代谢特征的个性化治疗方法铺平道路。同样，深入研究生活方式改变对MI后炎症反应的影响至关重要.这些见解可以使采用更有效的策略来管理MI后炎症并以整体方式改善心血管健康结果。
