Subjects Effector Results Reference
Rats with heart failure Sodium polysulthuionate Prevented decline in EF, reduced hypertrophy and pulmonary edema
attenuated fibrosis, prevented cardiac dilatation and cardiac contractile dysfunction; decreased BNP, enhanced Akt phosphorylation, and increased myocardial nitrate levels
Kondo K. et alCirculation. 2013 Mar 12;127(10):1116-27
Rats with high fat diet induced HF Sodium polysulthuionate Reverses high fat diet damage as observed by ejection fraction, fibrosis, and cardiac triglyceride; lowered blood glucose and serum insulin levels. Barr LA, et al Nitric Oxide. 2015 Apr 30;46:145-56.
Rats with heart failure NaHS H₂S protects heart during heart failure by suppression of local renin level through inhibition of both mast cell infiltration and renin degranulation. Liu YH, et al.. Antioxid Redox Signal 2014
Mice with heart failure Diallyl trisulfide H₂S improved left ventricular remodeling and preserved LV function in the setting of transverse aortic constriction while increasing vascular density Polhemus, D.J., et al. Circ Heart Fail, 2013. 6(5):
Mice with heart failure Na2S Upregulation of Trx1 by H₂S inhibits apoptosis signaling, which ultimately leads to the attenuation of left-ventricular remodeling. Nicholson CK, et al. Arter Throm Vasc Biol 2013
Mouse cardiac tissue NaHS H₂S via direct sulfhydration contributes to the beneficial effects in myocardial infarction-associated heart failure Nishida M, Sawa T, et al. Nat Chem Biol 2012
Rats with heart failure NaHS H₂S can significantly suppress cardiac hypertrophy and fibrosis induced by overloaded pressure by inhibiting intracardiac Ang-II and modifying Cx43. Huang J, Wang D, Zheng J, et al.. Mol Med Rep 2012
Rats with heart failure NaHS H₂S improved survival, increased the LVSP, decreased LVEDP, inhibited cardiac apoptosis in HF hearts and improved mitochondrial derangements
Mice with heart failure Na2S H₂S after MI protected structural and functional deterioration of the LV by attenuating oxidative stress and mitochondrial dysfunction. Calvert, J.W., et al., Circulation, 2010.
Mice with heart failure NaHS Administration of H₂S at the time of CPR markedly improves myocardial and neurological function and survival after cardiac arrest/CPR. Minamishima, S., et al., Circulation, 2009.
Chronic HF mice Sodium thiosulfate H₂S prevented ventricular contractile dysfunction with reduced aortic blood flow. H₂S modulated the extracellular matrix Sen U, Vacek TP, et al. Pharmacology 2008
Mice with heart failure Na2S Delivery of H₂S at the time of myocardial ischemia reperfusion limits infarct size and preserves left ventricular (LV) function. Elrod, J.W., et al., Proc Natl Acad Sci U S A, 2007.
Nrf2 deficient mice Na2S H₂S therapy enhances proteasomal activity and function during the development of heart failure in an Nrf2-dependent manner and that this enhancement leads to attenuation in cardiac dysfunction. Shimizu Y, et al. Circ Heart Fail. 2016
Rats with heart failure GYY4137 H₂S prodrug preserves cardiac function, attenuates adverse remodeling and may exert post-ischemic cardioprotective (pro-angiogenic, anti-apoptotic, anti-hypertrophic and anti-fibrotic) effects in part through enhanced early post-ischemic endogenous natriuretic peptide activation. Lilyanna S, et al. J Mol Cell Cardiol. 2015