Blood levels of cardiac troponins (cTn) and myoglobin are analysed when myocardial infarction (MI) is suspected. Here we describe a novel clearance mechanism for muscle proteins by muscle cells. The complete plasma clearance profile of cTn and myoglobin was followed in rats after intravenous or intermuscular injections and analysed by PET and fluorescence microscopy of muscle biopsies and muscle cells. Compared with intravenous injections, only 5 % of cTnT, 0.6 % of cTnI and 8 % of myoglobin were recovered in the circulation following intramuscular injection. In contrast, 47 % of the renal filtration marker FITC-sinistrin and 81 % of cTn fragments from MI-patients were recovered after intramuscular injection. In addition, PET and biopsy analysis revealed that cTn was taken up by the quadriceps muscle and both cTn and myoglobin were endocytosed by cultured muscle cells. This local clearance mechanism could possibly be the dominant clearance mechanism for cTn, myoglobin and other muscle damage biomarkers released by muscle cells.

当怀疑心肌梗塞 (MI) 时，分析心肌肌钙蛋白 (cTn) 和肌红蛋白的血液水平。在这里，我们描述了肌肉细胞对肌肉蛋白质的新清除机制。静脉或肌肉间注射后，在大鼠中跟踪 cTn 和肌红蛋白的完整血浆清除曲线，并通过 PET 和肌肉活检和肌肉细胞的荧光显微镜进行分析。与静脉注射相比，肌肉注射后循环中仅回收了 5% 的 cTnT、0.6% 的 cTnI 和 8% 的肌红蛋白。相比之下，来自 MI 患者的 47% 的肾脏过滤标志物 FITC-sinistrin 和 81% 的 cTn 片段在肌肉注射后被回收。此外，PET 和活检分析显示 cTn 被股四头肌吸收，cTn 和肌红蛋白都被培养的肌肉细胞内吞。这种局部清除机制可能是肌细胞释放的 cTn、肌红蛋白和其他肌肉损伤生物标志物的主要清除机制。