Myocardial infarction (MI) is a serious acute cardiovascular syndrome that causes myocardial injury due to blood flow obstruction to a specific myocardial area. Under ischemic–reperfusion settings, a burst of reactive oxygen species is generated, leading to redox imbalance that could be attributed to several molecules, including myoglobin. Myoglobin is dynamic and exhibits various oxidation–reduction states that have been an early subject of attention in the food industry, specifically for meat consumers. However, rarely if ever have the myoglobin optical properties been used to measure the severity of MI. In the current study, we develop a novel imaging pipeline that integrates tissue clearing, confocal and light sheet fluorescence microscopy, combined with imaging analysis, and processing tools to investigate and characterize the oxidation–reduction states of myoglobin in the ischemic area of the cleared myocardium post-MI. Using spectral imaging, we have characterized the endogenous fluorescence of the myocardium and demonstrated that it is partly composed by fluorescence of myoglobin. Under ischemia–reperfusion experimental settings, we report that the infarcted myocardium spectral signature is similar to that of oxidized myoglobin signal that peaks 3 h post-reperfusion and decreases with cardioprotection. The infarct size assessed by oxidation–reduction imaging at 3 h post-reperfusion was correlated to the one estimated with late gadolinium enhancement MRI at 24 h post-reperfusion. In conclusion, this original work suggests that the redox state of myoglobin can be used as a promising imaging biomarker for characterizing and estimating the size of the MI during early phases of reperfusion.

心肌梗死（MI）是一种严重的急性心血管综合征，由于特定心肌区域的血流受阻而导致心肌损伤。在缺血再灌注环境下，会产生大量活性氧，导致氧化还原失衡，这可能归因于包括肌红蛋白在内的多种分子。肌红蛋白是动态的，并表现出各种氧化还原状态，这已成为食品行业（特别是肉类消费者）早期关注的主题。然而，很少使用肌红蛋白的光学特性来测量心肌梗死的严重程度。在当前的研究中，我们开发了一种新颖的成像流程，集成了组织透明、共焦和光片荧光显微镜，结合成像分析和处理工具来研究和表征透明心肌缺血区域中肌红蛋白的氧化还原状态心肌梗死后。使用光谱成像，我们表征了心肌的内源性荧光，并证明它部分由肌红蛋白的荧光组成。在缺血再灌注实验环境下，我们报告梗塞心肌光谱特征与氧化肌红蛋白信号相似，该信号在再灌注后 3 小时达到峰值，并随着心脏保护而降低。再灌注后 3 小时通过氧化还原成像评估的梗塞面积与再灌注后 24 小时通过晚期钆增强 MRI 评估的梗塞面积相关。总之，这项原创工作表明，肌红蛋白的氧化还原状态可以用作一种有前途的成像生物标志物，用于表征和估计再灌注早期阶段 MI 的大小。