旨在探讨Mettl1在脓毒症心肌病中的作用及其机制，分析其对铜死亡机制的影响。20只SPF级C57BL/6N小鼠被随机分为模型组（n ＝ 10）和对照组（n ＝ 10），模型组通过腹腔注射脂多糖（lipopolysaccharide, LPS） （10 mg/kg）构建脓毒症心肌病。通过超声心动图评估心功能，并采用HE染色、流式细胞术、酶联免疫吸附试验（enzyme linked immunosorbent assay, ELISA）、实时荧光定量PCR（quantitative real-time polymerase chain reaction, qRT-PCR）和蛋白质印迹（western blotting, WB）等技术分析心肌病理变化、炎症因子及Mettl1、Wdr4、Fdx1和Akt基因的表达。与正常组相比，模型组小鼠的左心室射血分数（left ventricular ejection fraction, LVEF）、左心室缩短分数（left ventricular fractional shortening, LVFS）和左室收缩末期内径（left ventricular end systolic diameter, LVESD）显著降低（P < 0.01），心肌组织破坏明显，Mettl1、Fdx1、Wdr4和Akt的mRNA表达水平也显著升高。Mettl1沉默后，脓毒症心肌细胞的炎症因子TNF-α、IL-6和氧化应激指标MDA和ROS水平显著降低（P <0.01），且Wdr4、Fdx1和Akt基因表达水平显著降低（P < 0.01）。Mettl1在脓毒症心肌病中铜死亡信号通路发挥重要作用，沉默Mettl1可减轻心肌细胞炎症和氧化应激水平并调控铜死亡信号相关Wdr4、Fdx1和Akt基因表达水平，提示其作为潜在治疗靶点的价值。

This study aimed to explore the role and mechanism of Mettl1 in septic cardiomyopathy, and analyze its effect on the mechanism of cuproptosis. The impact of 20 SPF grade C57BL/6N mice were randomly divided into model group (n=10) and control group (n=10). The model group was treated with intraperitoneal injection of LPS (10 mg/kg) to construct septic cardiomyopathy. Cardiac function was assessed by echocardiography, and myocardial pathological changes, inflammatory factors and the expression of Mettl1, Wdr4, Fdx1 and Akt genes were analyzed by HE staining, flow cytometry, enzyme linked immunosorbent assay (ELISA), quantitative real-time polymerase chain reaction (qRT-PCR), western blotting (WB) and other techniques. Compared with the normal group, the left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS) and left ventricular end systolic diameter (LVESD) of the model group mice are significantly reduced (P < 0.01), and myocardial tissue damage is significant. The mRNA expressions of Mettl1, Fdx1, Wdr4 and Akt are also significantly increased. After silencing Mettl1, the levels of inflammatory factors TNF-α, IL-6 and oxidative stress indicators MDA and ROS in septic cardiomyocytes are significantly decreased (P < 0.01), and the gene expression levels of Wdr4, Fdx1 and Akt are significantly decreased (P < 0.01). Mettl1 plays an important role in cuproptosis signaling pathway in septic cardiomyopathy. Silencing Mettl1 can reduce the levels of inflammation and oxidative stress in cardiomyocytes and regulate the expression levels of Wdr4, Fdx1 and Akt genes related to cuproptosis signaling, suggesting its value as a potential therapeutic target.