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Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR
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Connective tissue growth factor inhibition attenuates left ventricular remodeling and dysfunction in pressure

Zoltán Szabó1, Johanna Magga, Tarja Alakoski

  • 1University of Oulu, Department of Pharmacology and Toxicology, P.O. Box 5000, FIN-90220 Oulu, Finland. Risto.Kerkela@oulu.fi.

Hypertension (Dallas, Tex. : 1979)
|April 2, 2014
PubMed

Insights

Blocking connective tissue growth factor (CTGF) with a monoclonal antibody (mAb) protected mouse hearts from pressure overload-induced dysfunction and remodeling. This suggests CTGF antagonism may prevent cardiac damage in hypertension.

Area of Science:

  • Cardiovascular Research
  • Fibrosis Pathogenesis
  • Molecular Cardiology

Background:

  • Connective tissue growth factor (CTGF) is implicated in fibrotic disorders, but its cardiac role remains unclear.
  • Cardiac fibrosis and heart failure are significant health concerns, necessitating research into underlying mechanisms.

Purpose of the Study:

  • To investigate the role of CTGF in cardiac fibrosis and heart failure development.
  • To evaluate the therapeutic potential of CTGF antagonism in pressure overload-induced cardiac remodeling.

Main Methods:

  • Mice underwent thoracic aortic constriction (TAC) or angiotensin II infusion.
  • CTGF function was antagonized using a CTGF monoclonal antibody (mAb).
  • Cardiac function, hypertrophy, fibrosis, and gene expression were assessed after 8 weeks.

Main Results:

  • CTGF mAb treatment preserved left ventricular (LV) systolic function and reduced LV dilatation post-TAC.
  • CTGF mAb treatment decreased cardiomyocyte size and hypertrophic gene expression.
  • CTGF mAb reduced collagen 1 production but did not significantly alter interstitial fibrosis post-TAC.
  • CTGF antagonism did not affect LV dysfunction or hypertrophy in angiotensin II-infused mice.

Conclusions:

  • CTGF mAb protects against adverse LV remodeling and dysfunction in pressure overload models (TAC).
  • CTGF antagonism shows promise in preventing cardiac end-organ damage associated with hypertension.
Keywords:
connective tissue growth factorfibrosishypertrophy, left ventricularventricular dysfunction, leftventricular remodeling

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