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October 9, 2025Circulation Research

Abstract Wed010: Endothelial NFATc3 improved angiogenesis after myocardial infarction by upregulating lncRNA MALAT1 to promote mitochondrial function

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Authors

FHFangze HuangMZMengru ZhengRLRanxin Liu

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Overview

Observational analysis reports that NFATc3 enhances angiogenesis in endothelial cells after myocardial infarction, indicating its therapeutic potential.

Key Points

  • NFATc3 promotes angiogenesis in endothelial cells, thereby mitigating cardiac injury after myocardial infarction.
  • Deletion of NFATc3 in endothelial cells impacts mitochondrial function and reduces angiogenesis, worsening heart damage.
  • NFATc3 upregulates lncRNA MALAT1, which is crucial for enhancing mitochondrial function in endothelial cells.
  • Targeting NFATc3 in endothelial cells offers a novel therapeutic strategy for myocardial infarction treatment.

Cite This Study

Huang et al. (2025) studied this question.

synapsesocial.com/papers/68e77f09d1c187e1c108fc0ahttps://doi.org/10.1161/res.137.suppl_1.wed010
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  1. 1Abstract Thu097: METTL3 inhibition reduces myofibroblast activation and adverse remodeling following MI.2025
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  4. 4NEAT1 Coordinates a PDLIM5–CACNA1C Regulatory Program Associated with a Potentially Arrhythmogenic Cardiomyocyte State in the Border Zone During Early Myocardial Infarction2026
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