State Key Laboratory of Biocatalysis and Enzyme Engineering, School of Life Sciences, Hubei University, Wuhan, China.
Department of Biological Repositories, Frontier Science Center for Immunology and Metabolism, Medical Research Institute, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China.
Nat Commun. 2024 Sep 12;15(1):7996. doi: 10.1038/s41467-024-52221-9.
Advancements in human-engineered heart tissue have enhanced the understanding of cardiac cellular alteration. Nevertheless, a human model simulating pathological remodeling following myocardial infarction for therapeutic development remains essential. Here we develop an engineered model of myocardial repair that replicates the phased remodeling process, including hypoxic stress, fibrosis, and electrophysiological dysfunction. Transcriptomic analysis identifies nine critical signaling pathways related to cellular fate transitions, leading to the evaluation of seventeen modulators for their therapeutic potential in a mini-repair model. A scoring system quantitatively evaluates the restoration of abnormal electrophysiology, demonstrating that the phased combination of TGFβ inhibitor SB431542, Rho kinase inhibitor Y27632, and WNT activator CHIR99021 yields enhanced functional restoration compared to single factor treatments in both engineered and mouse myocardial infarction model. This engineered heart tissue repair model effectively captures the phased remodeling following myocardial infarction, providing a crucial platform for discovering therapeutic targets for ischemic heart disease.
人工心脏组织的进步增强了我们对心脏细胞变化的理解。然而,模拟心肌梗死后病理性重构的人类模型对于治疗开发仍然至关重要。在这里,我们开发了一种心肌修复的工程模型,可复制包括缺氧应激、纤维化和电生理功能障碍在内的阶段性重塑过程。转录组分析确定了与细胞命运转变相关的九个关键信号通路,从而评估了十七种调节剂在小型修复模型中的治疗潜力。评分系统定量评估了异常电生理的恢复情况,表明 TGFβ 抑制剂 SB431542、Rho 激酶抑制剂 Y27632 和 WNT 激活剂 CHIR99021 的阶段性组合治疗比单一因素治疗在工程化和小鼠心肌梗死模型中均能更有效地恢复功能。这种工程心脏组织修复模型有效地捕获了心肌梗死后的阶段性重塑,为发现缺血性心脏病的治疗靶点提供了一个关键平台。