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KLF15-Wnt-Dependent Cardiac Reprogramming Up-Regulates SHISA3 in the Mammalian Heart.

Claudia Noack1, Lavanya M Iyer2, Norman Y Liaw3

  • 1Institute of Pharmacology and Toxicology, University Medical Center Goettingen, Georg-August University, Goettingen, Germany; DZHK (German Center for Cardiovascular Research), partner site Goettingen, Germany; Research & Development, Pharmaceuticals, Bayer AG, Berlin, Germany.

Journal of the American College of Cardiology
|October 5, 2019
PubMed
Summary

KLF15 regulates heart failure by controlling cardiomyocyte and vascular cell remodeling. This study identified SHISA3 as a novel therapeutic target for heart failure, conserved across species.

Keywords:
Wnt signalingfetal gene reprogrammingheart failurehypertrophic heart remodelingvascular cells

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Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Transcriptional Regulation

Background:

  • Fetal reprogramming of cardiomyocytes (CM) and vascular cells (VC) contributes to heart failure (HF).
  • KLF15 is implicated as a key regulator of CM hypertrophy in HF.
  • Mechanisms underlying CM-VC interactions in HF progression remain incompletely understood.

Purpose of the Study:

  • To investigate KLF15-dependent transcriptional networks in cardiac remodeling and HF.
  • To identify therapeutic targets for HF intervention in adult hearts.
  • To elucidate the role of CM-VC crosstalk in HF pathogenesis.

Main Methods:

  • Transcriptomic bioinformatics analysis.
  • Phenotyping of Klf15 knockout mice.
  • Utilized pressure overload and myocardial ischemia models.
  • Employed engineered human myocardium and stem cells for validation.

Main Results:

  • KLF15 mediates postnatal transcriptional repression of pathological remodeling pathways.
  • Identified a CM-initiated vascular program involving reduced KLF15 and activated Wnt signaling.
  • Discovered SHISA3, a novel VC-expressed gene, as a conserved player in pathological remodeling.

Conclusions:

  • KLF15-Wnt dynamics govern CM and VC homeostasis, offering a therapeutic target for HF.
  • SHISA3 is a novel, evolutionarily conserved VC marker associated with pathological remodeling in HF.