Intermedin1–53 enhances angiogenesis and attenuates adverse remodeling following myocardial infarction by activating AMP-activated protein kinase

@inproceedings{Chen2017Intermedin153EA,
  title={Intermedin1–53 enhances angiogenesis and attenuates adverse remodeling following myocardial infarction by activating AMP-activated protein kinase},
  author={Kankai Chen and Meiling Yan and Yongguang Li and Zhifeng Dong and Dong Huang and Jingbo Li and Meng Wei},
  booktitle={Molecular medicine reports},
  year={2017}
}
Adverse ventricular remodeling is a maladaptive response to acute loss of myocardium and an important risk factor for heart failure following myocardial infarction (MI). Intermedin (IMD) is a novel member of the calcitonin/calcitonin gene‑related peptide family, which may possess potent cardioprotective properties. The aim of the present study was to determine whether IMD1‑53, a mature bioactive form of IMD, may promote therapeutic angiogenesis within the infarcted myocardium, therefore… CONTINUE READING
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