Key result
Targeting stress-induced transcriptional changes in the heart could be an effective therapeutic strategy for left ventricular hypertrophy, requiring consideration of timing and target specificity.
Understanding and targeting the transcriptional regulators of long-term changes in LVH is a crucial step in identifying novel therapeutic targets to prevent or reverse maladaptive cardiac remodeling.
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May inform transcriptional targeting strategies in LVH; leaves open optimal timing and specificity for clinical translation.
In most clinical cases, left ventricular hypertrophy (LVH) occurs over time from persistent cardiac stress. At the molecular level, this results in both transient and long-term changes to metabolic, sarcomeric, ion handling, and stress signaling pathways. Although this is initially an adaptive change, the mechanisms underlying LVH eventually lead to maladaptive changes including fibrosis, decreased cardiac function, and failure. Understanding the regulators of long-term changes, which are largely driven by transcriptional remodeling, is a crucial step in identifying novel therapeutic targets for preventing the downstream negative effects of LVH and treatments that could reverse or prevent it. The development of effective therapeutics, however, will require a critical understanding of what to target, how to modify important pathways, and how to identify the stage of pathology in which a specific treatment should be used.
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Nam et al. (2017) conducted a review in Left Ventricular Hypertrophy. Transcriptional targeted therapies was evaluated. Targeting stress-induced transcriptional changes in the heart could be an effective therapeutic strategy for left ventricular hypertrophy, requiring consideration of timing and target specificity.
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