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STAT5b is a key effector of NRG-1/ERBB4-mediated myocardial growth. | LitMetric

AI Article Synopsis

  • Neuregulin-1 (NRG-1) is being researched as a potential treatment for heart failure, and it stimulates growth in heart cells (cardiomyocytes) through a pathway involving the protein STAT5b.
  • Disruption of the NRG-1/ERBB4 pathway reduces STAT5b's activation and leads to decreased expression of important growth-related genes, negatively impacting cardiomyocyte growth and hypertrophy (enlargement).
  • Research in model organisms like zebrafish and genetically modified mice shows that inhibiting the NRG-1/ERBB4 pathway or the protein Dynamin-2 significantly hinders heart growth and function, highlighting differences in this signaling pathway between healthy individuals and those with heart disease

Article Abstract

The growth factor Neuregulin-1 (NRG-1) regulates myocardial growth and is currently under clinical investigation as a treatment for heart failure. Here, we demonstrate in several in vitro and in vivo models that STAT5b mediates NRG-1/EBBB4-stimulated cardiomyocyte growth. Genetic and chemical disruption of the NRG-1/ERBB4 pathway reduces STAT5b activation and transcription of STAT5b target genes Igf1, Myc, and Cdkn1a in murine cardiomyocytes. Loss of Stat5b also ablates NRG-1-induced cardiomyocyte hypertrophy. Dynamin-2 is shown to control the cell surface localization of ERBB4 and chemical inhibition of Dynamin-2 downregulates STAT5b activation and cardiomyocyte hypertrophy. In zebrafish embryos, Stat5 is activated during NRG-1-induced hyperplastic myocardial growth, and chemical inhibition of the Nrg-1/Erbb4 pathway or Dynamin-2 leads to loss of myocardial growth and Stat5 activation. Moreover, CRISPR/Cas9-mediated knockdown of stat5b results in reduced myocardial growth and cardiac function. Finally, the NRG-1/ERBB4/STAT5b signaling pathway is differentially regulated at mRNA and protein levels in the myocardium of patients with pathological cardiac hypertrophy as compared to control human subjects, consistent with a role of the NRG-1/ERBB4/STAT5b pathway in myocardial growth.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10157316PMC
http://dx.doi.org/10.15252/embr.202256689DOI Listing

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