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Cardiovascular disease

PDE9A inhibition mends broken hearts

Nature Reviews Drug Discovery volume 14, pages 310–311 (2015)Cite this article

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Increases in cGMP levels are triggered by two independent factors: nitric oxide (NO) and atrial natriuretic peptide (ANP). PDE5A hydrolyses NO-coupled cGMP, but NO signalling is downregulated in heart disease, which might help to explain the lack of efficacy of PDE5A inhibition. Which PDEs are responsible for degrading cGMP resulting from ANP stimulation was not clear, and so the authors investigated the activity of the other cGMP-selective PDE, PDE9A, in the heart.

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References

  1. Lee, D. I. et al. Phosphodiesterase 9A controls nitric-oxide-independent cGMP and hypertrophic heart disease. Nature 519, 472–476 (2015)

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  1. Natasha Bray
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Bray, N. PDE9A inhibition mends broken hearts. Nat Rev Drug Discov 14, 310–311 (2015). https://doi.org/10.1038/nrd4618

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  • DOI: https://doi.org/10.1038/nrd4618

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