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A Rat Model of Pressure Overload Induced Moderate Remodeling and Systolic Dysfunction as Opposed to Overt Systolic Heart Failure
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A Rat Model of Pressure Overload Induced Moderate Remodeling and Systolic Dysfunction as Opposed to Overt Systolic Heart Failure

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Molecular pathogenesis of myocardial remodeling and new potential therapeutic targets in chronic heart failure

Giuseppe Distefano1, Pietro Sciacca

  • 1Department of Pediatrics, Pediatric Cardiology Service, University of Catania, Via S Sofia 78, Catania, 95123, Italy. distef@unict.it

Italian Journal of Pediatrics
|September 14, 2012
PubMed

Insights

Chronic heart failure (CHF) involves progressive cardiac dysfunction due to myocardial remodeling. New therapies targeting anti-apoptosis, anti-fibrosis, gene, and regenerative medicine offer hope for regression.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Regenerative Medicine

Background:

  • Chronic heart failure (CHF) natural history is marked by progressive cardiac dysfunction resistant to standard treatments.
  • Myocardial remodeling, a complex ultrastructural rearrangement, is the primary driver of CHF's negative clinical progression.
  • Remodeling involves cardiomyocyte hypertrophy, apoptosis, extracellular matrix changes, fibrosis, and altered gene expression.

Purpose of the Study:

  • To explore novel therapeutic strategies for reversing myocardial remodeling in CHF.
  • To review the potential of antiapoptotic and antifibrotic agents.
  • To discuss the prospects of myocardial gene and regenerative therapy.

Main Methods:

  • Literature review of studies on CHF, myocardial remodeling, and emerging therapies.
  • Analysis of molecular and cellular mechanisms underlying myocardial remodeling.
  • Evaluation of preclinical and clinical data on therapeutic interventions.

Main Results:

  • Myocardial remodeling is a central pathological process in CHF progression.
  • Several molecular targets within the remodeling cascade have been identified.
  • Apoptosis and fibrosis are key components of remodeling amenable to therapeutic intervention.

Conclusions:

  • Targeting myocardial remodeling offers a promising therapeutic avenue for CHF.
  • Antiapoptotic and antifibrotic agents show potential for mitigating CHF progression.
  • Myocardial gene and regenerative therapies represent future frontiers in CHF treatment.

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