Small molecules that control signal transduction pathways directed at transcription factors and chromatin-modifying enzymes represent a potential strategy for normalizing gene expression in heart failure.
Highlights the potential of targeting gene expression pathways with small molecules as a therapeutic approach for heart failure.
In response to acute and chronic stresses, the heart frequently undergoes a remodeling process that is accompanied by myocyte hypertrophy, impaired contractility, and pump failure, often culminating in sudden death. The existence of redundant signaling pathways that trigger heart failure poses challenges for therapeutic intervention. Cardiac remodeling is associated with the activation of a pathological gene program that weakens cardiac performance. Thus, targeting the disease process at the level of gene expression represents a potentially powerful therapeutic approach. In this review, we describe strategies for normalizing gene expression in the failing heart with small molecules that control signal transduction pathways directed at transcription factors and associated chromatin-modifying enzymes.
McKinsey et al. (Tue,) conducted a review in Heart failure. Small molecules targeting transcription factors and chromatin-modifying enzymes was evaluated. Small molecules that control signal transduction pathways directed at transcription factors and chromatin-modifying enzymes represent a potential strategy for normalizing gene expression in heart failure.
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