Key result
Targeting the disease process at the level of gene expression with small molecules that control signal transduction pathways represents a potentially powerful therapeutic approach for heart failure.
Modulating chromatin-modifying enzymes and transcription factors with small molecules represents a promising future therapeutic strategy for heart failure.
May support small-molecule gene-expression targeting in HF; leaves open need for clinical validation.
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.
No takes yet. Share an insight, caveat, or question.
McKinsey et al. (2005) conducted a review in Heart failure and cardiac hypertrophy. Transcriptional therapies (e.g., HDAC inhibitors, calcineurin/NFAT modulators) was evaluated. Targeting the disease process at the level of gene expression with small molecules that control signal transduction pathways represents a potentially powerful therapeutic approach for heart failure.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: