Project description:Myocardial infarction models developed to understand fibrosis and promote myocardial regeneration towards ischemic heart disease (IHD) is challenged due to the low-throughput nature of in vivo models and the lack of humanized cardiac scarring in the in vitro models. We generated a novel 4D cardiac scarring model (4DCSM) mimicking the IHD in vitro based on the human engineered heart tissue(hEHT). To identify potential signaling dominating the fibrotic process, we characterized transcriptomics of 4DCSM at different scarring stages by single-cell RNA sequencing. Taken together, our dataset is an informative resource to reveal the critical cell-types fate transformation and in fibrotic process and provides potential comparisons with public clinical data cohorts or other MI fibrosis model data.
Project description:Myocardial infarction models developed to understand fibrosis and promote myocardial regeneration towards ischemic heart disease (IHD) is challenged due to the low-throughput nature of in vivo models and the lack of humanized cardiac scarring in the in vitro models. We generated a novel 4D cardiac scarring model (4DCSM) mimicking the IHD in vitro based on the human engineered heart tissue(hEHT). To identify potential signaling dominating the fibrotic process, we characterized transcriptomics of 4DCSM at different scarring stages by bulk RNA sequencing. Taken together, our dataset is an informative resource to reveal the potential signaling dominating the fibrotic process and provides potential comparisons with public clinical data cohorts or other MI fibrosis model data.
Project description:Impact statementReducing ischemia-reperfusion injury would significantly improve patient survival. Current preclinical models are inadequate because they rely on animals, which do not emulate human physiology and the clinical setting. We developed a human tissue platform that allowed us to assess the human cardiac response, and demonstrated the platform's utility by measuring injury during ischemia-reperfusion and the effects of cardioprotective strategies. The model provides a foundation for future studies on how patient-specific backgrounds may affect response to therapeutic strategies. These steps will be necessary to help translate therapies into the clinical setting.
