Chronic inhibition of cyclic GMP phosphodiesterase 5A prevents and reverses cardiac hypertrophy

By E. Takimoto, H. Champion, Manxiang Li, Diego Belardi, Shuxun Ren, E. Rodriguez, D. Bedja, K. Gabrielson, Yibin Wang, D. Kass. Nature Medicine, 2005

937 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/1724d579b7e59490aaf62a21b3c29200fa5d7975

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cardiology and Cardiovascular Medicine

1. Barry A. Borlaug
2. W. Paulus
3. C. Tschöpe
4. J. Heineke
5. J. Molkentin

In Molecular Biology

1. J. Heineke
2. V. Bronte
3. W. Paulus
4. C. Tschöpe
5. J. Molkentin

Citations in the corpus

• A novel paradigm for heart failure with preserved ejection fraction: comorbidities drive myocardial dysfunction and remodeling through coronary microvascular endothelial inflammation. (2013, positive): “…mice subjected to transverse aortic constriction, sildena fi l, which increases myocardial PKG activity through inhibited breakdown of cGMP by phosphodiesterase 5 (PDE5), prevented or reversed cardiomyocyte hypertrophy and interstitial fi brosis by deactivating multiple prohypertrophic pathways (43).”
• Heart failure with preserved ejection fraction: pathophysiology, diagnosis, and treatment. (2011, background): “Validation of these diagnostic guidelines for HFpEF is urgently needed.101 Valuable validation efforts of the last set of guidelines provided by the Heart Failure and Echocardiography Associations of the European Society of Cardiology have to some extent been addressed, including: (i) the diagnostic”
• Regulation of cardiac hypertrophy by intracellular signalling pathways (2006, background): “As well as the antihypertrophic properties of GSK3β and class II HDACs (see above), cytosolic phospholipase A2 (cPLA2) and the cyclic GMP-dependent protein kinase-I (PKGI) have critical function”
• Effect of Phosphodiesterase-5 Inhibition on Exercise Capacity and Clinical Status in Heart Failure with Preserved Ejection Fraction: A Randomized Clinical Trial (2013, neutral): “Medial E/e' 90 17 (12-24) 98 15 (10-23) 16 (11-23)”
• Phosphodiesterase-5 inhibition augments endogenous antitumor immunity by reducing myeloid-derived suppressor cell function (2006, background): “By increasing the intracellular concentrations of cyclic guanosine monophosphate (cGMP), phosphodiesterase-5 (PDE5) inhibitors such as sildenafi l (Viagra), vardenafi l (Levitra), and tadalafi l (Cialis) have been used therapeutically to treat erectile dysfunction (12), pulmonary hypertension (13), ”