Spatial Transcriptional Heterogeneity in the Infarct Core and Its Surrounding Regions Targeting Piezo1 Signals in Rats With Myocardial Ischemia‐Reperfusion Injury

压电1 免疫印迹 细胞生物学 转录组 免疫荧光 生物 调解人 细胞 北方斑点 心肌梗塞 细胞内 免疫组织化学 污渍 基因表达 化学 左心室 病理 心内膜 分子生物学 解剖 小RNA 医学
作者
Zhen Li,Fan Jiang,Yan Chen,Zhixiao Li,Yanqiong Wu,Zhigang He,Duozhi Wu,Hongbing Xiang
出处
期刊:MedComm [Wiley]
卷期号:7 (1): e70537-e70537 被引量:2
标识
DOI:10.1002/mco2.70537
摘要

ABSTRACT Myocardial ischemia‐reperfusion (MIR) injury is a major cause of cardiac dysfunction, but the spatial heterogeneity of its underlying molecular programs remains unclear. In this study, we applied Visium spatial transcriptomics to generate gene expression maps of rat left ventricles after MIR and identified distinct regional features. The border zones were enriched with phagosome‐related genes, incomplete infarct areas showed activation of MAPK, IL‐17, and osteoclast differentiation pathways, while the infarct cores were characterized by ferroptosis and mitophagy‐related genes. To further resolve the cellular basis, we integrated single‐cell RNA sequencing with RCTD deconvolution and found immune cell infiltration in infarct zones, neutrophil enrichment in incomplete infarct areas, and smooth muscle cell predominance in border zones. Both spatial and single‐cell analyses revealed altered expression of Piezo1, RyR2, MMP2, and SERCA2, which was further validated by Western blot and immunofluorescence co‐staining with ACTN2. Pseudotime analysis demonstrated selective enrichment and dynamic activation of Piezo1 in specific cardiomyocyte subclusters. Functional validation using a hypoxia/reoxygenation model confirmed that reoxygenation induced marked intracellular Ca 2+ accumulation, which was attenuated by the Piezo1 inhibitor GsMTx4. Together, these findings delineate the spatial heterogeneity of MIR injury, identify Piezo1 as a key mediator of Ca 2+ dysregulation, and suggest Piezo1 as a potential therapeutic target for myocardial protection.
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