Urocortin 3 Gene Transfer Increases Function of the Failing Murine Heart

Dimosthenis Giamouridis, Mei Hua Gao, N. Chin Lai, Zhen Tan, Young Chul Kim, Tracy Guo, Atsushi Miyanohara, Matthijs W. Blankesteijn, Erik A. L. Biessen, H. Kirk Hammond*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

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Abstract

Peptide infusions of peptides the corticotropin releasing factor family, including urocortin 2, stresscopin, and urocortin 3 (UCn3), have favorable acute effects in clinical heart failure (HF), but their short half-lives make them unsuitable for chronic therapy. This study asked whether UCn3 gene transfer, which provides sustained elevation of plasma UCn3 levels, increases the function of the failing heart. HF was induced by transmural left ventricular (LV) cryoinjury in mice. LV function was assessed 3 weeks later by echocardiography. Those with ejection fractions (EF)

Original languageEnglish
Pages (from-to)10-20
Number of pages11
JournalHuman Gene Therapy
Volume30
Issue number1
DOIs
Publication statusPublished - Jan 2019

Keywords

  • gene therapy
  • heart failure with reduced EF
  • SERCA2a
  • AAV8
  • ADENOASSOCIATED VIRUS VECTORS
  • MYOCARDIAL-INFARCTION
  • FAILURE
  • PHARMACOKINETICS
  • DYSFUNCTION
  • EXPRESSION
  • MUSCLE
  • MOUSE

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