2017
DOI: 10.1111/bph.13688
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Abstract: AP39 protects against reperfusion injury independently of the cytosolic RISK pathway. This cardioprotective effect could be mediated by inhibiting PTP via a cyclophilin D-independent mechanism. Thus, selective delivery of H S to mitochondria may be therapeutically applicable for employing the cardioprotective utility of H S.

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Cited by 69 publications
(61 citation statements)
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“…Currently, AP39, which appears to be a more effective H 2 S releaser than AP123 (Gerö et al, 2016), has been studied more extensively. Interestingly, and consistently with the positive bioenergetic effects of low concentrations of H 2 S, low concentrations of AP39 (25-100 nM) induced an elevation in basal mitochondrial activity (basal respiration and maximal respiration) of cultured endothelial cells and neurons, whereas at higher concentrations (250-300 nM) this effect is no longer detectable (Szczesny et al, 2014;Zhao et al, 2016a), consistent with the bell-shaped mitochondrial action of H 2 S. Mitochondrial H 2 S delivery with AP39 improved mitochondrial function in oxidatively stressed cells, at least in part due to the fact that it reduced mitochondrial ROS levels (Szczesny et al, 2014;Karwi et al, 2017). In addition, AP39 and AP123 also improved mitochondrial DNA repair in oxidatively stressed cells (Szczesny et al, 2014, Ger} o et al, 2016.…”
Section: Mitochondrially Targeted H 2 S Donorsmentioning
confidence: 76%
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“…Currently, AP39, which appears to be a more effective H 2 S releaser than AP123 (Gerö et al, 2016), has been studied more extensively. Interestingly, and consistently with the positive bioenergetic effects of low concentrations of H 2 S, low concentrations of AP39 (25-100 nM) induced an elevation in basal mitochondrial activity (basal respiration and maximal respiration) of cultured endothelial cells and neurons, whereas at higher concentrations (250-300 nM) this effect is no longer detectable (Szczesny et al, 2014;Zhao et al, 2016a), consistent with the bell-shaped mitochondrial action of H 2 S. Mitochondrial H 2 S delivery with AP39 improved mitochondrial function in oxidatively stressed cells, at least in part due to the fact that it reduced mitochondrial ROS levels (Szczesny et al, 2014;Karwi et al, 2017). In addition, AP39 and AP123 also improved mitochondrial DNA repair in oxidatively stressed cells (Szczesny et al, 2014, Ger} o et al, 2016.…”
Section: Mitochondrially Targeted H 2 S Donorsmentioning
confidence: 76%
“…A potential advantage of mitochondrially targeted donors is that their effects are not dependent on the functional integrity of the NO system and do not involve activation of the cGMP/protein kinase G system (Tomasova et al, 2015;Chatzianastasiou et al, 2016;Karwi et al, 2017). However, actions through Ca V 3, RyR2, and Clcardiac membrane channels have been implicated in its pharmacological actions (Tomasova et al, 2015), perhaps related to the accumulation of AP39 in the nodal cells due to the high positive charge of the compound and high negative resting potential of the nodal cells.…”
Section: Mitochondrially Targeted H 2 S Donorsmentioning
confidence: 99%
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“…S-nitrosation temporarily locks complex I in the deactive state, preventing RET upon reperfusion, but as the modification is reversible, the activity of complex I is restored to normal a few minutes after reperfusion 141 . It is likely that many other agents that protect against IR injury, such as hydrogen sulfide 142,143 , act in a similar way to decrease ROS production upon reperfusion 114 .…”
Section: Ischemia-reperfusion Injurymentioning
confidence: 99%
“…Myocardial biopsies were collected at the end of perfusion for biochemical characterization, as previously described. [27][28][29] Briefly, protein samples (30 μg/well) were loaded onto 10% SDS-PAGE to be separated based on molecular weight, and were then transferred onto a nitrocellulose membrane using a wet-transfer method. The membrane was incubated with one of the following primary antibodies…”
Section: Immunoblotting Analysismentioning
confidence: 99%