Transient receptor potential melastatin 7 (TRPM7), a non-selective cation channel, was significantly upregulated in the blood of patients with sepsis. This study focuses on the preliminary exploration of the probable regulatory mechanism of TRPM7 in sepsis-induced myocardial injury (SIMI). HL-1 cardiac muscle cell line was treated with lipopolysaccharide (LPS) to mimic SIMI in vitro, and TRPM7 level was assessed. The impacts of TRPM7 knockdown on cellular inflammation response, oxidative stress, apoptosis, endoplasmic reticulum (ER) stress, and ferroptosis were identified. In order to explore the mechanism, ER stress agonist tunicamycin (TM) or ferroptosis inducer erastin was applied to treat HL-1 cells. The influences of TM and erastin on the aforementioned aspects were evaluated. TRPM7 was elevated in response to LPS stimulation, and its knockdown reduced the secretion of inflammatory factors and oxidative stress degree. Moreover, TRPM7 knockdown significantly suppressed cell apoptosis, ER stress, and ferroptosis. TM and erastin reversed the functions of TRPM7 knockdown, indicating ER stress and ferroptosis mediated in the regulation of TRPM7. This research proposes the possibility of TRPM7 as a marker or target for SIMI, and provides theoretical support for follow-up research.

瞬时受体电位褪黑素 7 (TRPM7) 是一种非选择性阳离子通道，在脓毒症患者的血液中显着上调。本研究重点初步探索TRPM7在脓毒症引起的心肌损伤（SIMI）中可能的调节机制。用脂多糖 (LPS) 处理 HL-1 心肌细胞系以在体外模拟 SIMI，并评估 TRPM7 水平。确定了 TRPM7 敲低对细胞炎症反应、氧化应激、细胞凋亡、内质网 (ER) 应激和铁死亡的影响。为了探讨其机制，应用ER应激激动剂衣霉素（TM）或铁死亡诱导剂erastin处理HL-1细胞。评估了TM和erastin对上述方面的影响。TRPM7 因 LPS 刺激而升高，其敲低可降低炎症因子的分泌和氧化应激程度。此外，TRPM7 敲低显着抑制细胞凋亡、内质网应激和铁死亡。TM和erastin逆转了TRPM7敲低的功能，表明ER应激和铁死亡在TRPM7的调节中介导。本研究提出了TRPM7作为SIMI标记物或靶点的可能性，为后续研究提供理论支持。