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Renin-angiotensin blockade combined with natriuretic peptide system augmentation: novel therapeutic concepts to combat heart failure.
TLDR
Despite encouraging results from many clinical trials, ACEi- and ARBs-based pharmacotherapy is still far from optimal, and ACEi may lose their efficacy over time because of redundant Ang-II–generating pathways and the so-called aldosterone escape.
Does indoxyl sulfate, a uraemic toxin, have direct effects on cardiac fibroblasts and myocytes?
TLDR
It is demonstrated for the first time that IS has pro-fibrotic, pro-hypertrophic, and pro-inflammatory effects, indicating that IS might play an important role in adverse cardiac remodelling mediated via activation of the p38 MAPK, p42/44MAPK, and NFkappaB pathways.
Angiotensin Receptor Neprilysin Inhibitor LCZ696 Attenuates Cardiac Remodeling and Dysfunction After Myocardial Infarction by Reducing Cardiac Fibrosis and Hypertrophy
TLDR
LCZ696 attenuated cardiac remodeling and dysfunction after experimental myocardial infarction and may be contributed to by superior inhibition of LCZ696 on cardiac fibrosis and cardiac hypertrophy than either stand-alone neprilysin inhibitor or angiotensin receptor blocker.
Inotropic responses to human gene 2 (B29) relaxin in a rat model of myocardial infarction (MI): effect of pertussis toxin
TLDR
Cardiac failure in MI animals caused a reduced inotropic response to both relaxin and (−)‐isoprenaline, and in non‐MI animals, PTX treatment significantly reduced relaxin‐, isoprenalin‐ and forskolin‐stimulated cAMP accumulation.
Cardiorenal Syndrome: The Emerging Role of Protein-Bound Uremic Toxins
TLDR
It is demonstrated that protein-bound uremic toxins may play an important role in progression of cardiovascular disease in the setting of chronic kidney disease and potential mechanisms underlying indoxyl sulfate−induced cardiorenal fibrosis are discussed.
Cardiac Tissue Engineering in an In Vivo Vascularized Chamber
TLDR
The use of a vascularized tissue-engineering chamber allowed generation of a spontaneously beating 3-dimensional mass of cardiac tissue from neonatal rat cardiomyocytes, which showed a typical cardiac muscle length-tension relationship, and the ability to be paced from electrical field pulses up to 3 Hz.
Differential Effect of Urotensin II on Vascular Tone in Normal Subjects and Patients With Chronic Heart Failure
TLDR
The contention that the U-II system may be a potentially important target for pharmacological blockade in the treatment of patients with chronic heart failure is supported.
Desensitization of cardiac beta-adrenoceptor signaling with heart failure produced by myocardial infarction in the rat. Evidence for the role of Gi but not Gs or phosphorylating proteins.
TLDR
Pertussis toxin treatment of animals restored inotropic responses to isoproterenol in left atria and left papillary muscle to levels seen in the sham group, indicating that inactivation of Gi-proteins improves inotropic function in MI rats, and that beta-ARs couple to Gi in cardiac failure.
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