既往研究显示，心肌梗死后其梗死区域内脂肪浸润的发生率较高，并且与不良预后密切相关，但对于其发生机制尚无报告。申请者在前期工作中率先发现，出血性心肌梗死慢性期的铁沉积与梗死心肌内的脂肪浸润有关；进一步研究发现，伴有铁沉积的梗死心肌内发生巨噬细胞浸润，氧化脂质水平增高，辅助极化M2型巨噬细胞的IL4、IL13表达水平升高。在此基础上，本项目拟通过磁共振定量分析明确梗死心肌内铁沉积与脂肪浸润的相关性，进而深入探索铁沉积介导脂肪浸润的机制，试图证明：沉积铁通过IL-4、IL-13辅助完成M2型巨噬细胞的极化；通过催化生成氧化脂质诱导M2型巨噬细胞膜上的SR-A高表达，进而吞噬氧化脂质转化成泡沫细胞；通过巨噬细胞膜上的Ferroportin1实现铁离子的价态还原及跨细胞膜循环。从而阐明铁沉积介导梗死心肌内脂肪浸润的生物学机制，为心肌梗死慢性期的治疗提供依据。

Previous studies have shown high prevalence of fat infiltration in infarcted myocardium post myocardial infarction, which was considered a predictor of poor prognosis. However, there is few reports on its mechanism. Our previous study showed that fat infiltration within infarcted myocardium post myocardial infarction was associated with regional iron deposition in chronic hemorrhagic myocardial infarction; study on the infarcted myocardium with iron deposition showed that: macrophages were recruited to infarcted territory, lipid peroxide increased, cytokines IL4 and IL13 that could polarize M2 macrophages increased..We try to use CMR-based quantification and histological verification to explore the correlation between iron deposition and fat infiltration within infarcted myocardium; furthermore, we will try to prove that iron ions polarize M2 macrophages with the help of IL4 and IL13; iron promote lipid peroxide that stimulate M2 macrophages highly expressed SR-A, MΦ2 phagocytose lipid peroxide with SR-A and turn into foam cells; M2 macrophages reduced F3+ and cycled iron across the cell membrane by high-expressed ferroportin1 and low-expressed ferritin-L. The results will be helpful in understanding the mechanism of fat infiltration within infarcted myocardium and establishing a treatment plan for chronic myocardial infarction.