Pyridine Dinucleotides from Molecules to Man

Fessel, Joshua P.; Oldham, William M.

doi:10.1089/ars.2017.7120

Cited by 27 publications

(26 citation statements)

References 289 publications

(309 reference statements)

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“…The deregulation might be because of problems in the metabolic system or toxicological challenge exposure, and might even further provoke metabolic error. 71 , 72 …”

Section: Mitochondrial Dynamics In Cardiac Ischemiamentioning

confidence: 99%

<p>Targeting Cardiac Metabolic Pathways: A Role in Ischemic Management</p>

Yehualashet¹,

Belachew²,

Kifle³

et al. 2020

VHRM

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Among the vast number of noncommunicable diseases encountered worldwide, cardiovascular diseases accounted for about 17.8 million deaths in 2017 and ischemic heart disease (IHD) remains the single-largest cause of death in countries across all income groups. Because conventional medications are not without shortcomings and patients still refractory to these medications, scientific investigation is ongoing to advance the management of IHD, and shows a great promise for better treatment modalities, but additional research can warrant improvement in terms of the quality of life of patients. Metabolic modulation is one promising strategy for the treatment of IHD, because alterations in energy metabolism are involved in progression of the disease. Therefore, the purpose of this review was to strengthen attention toward the use of metabolic modulators and to review the current level of knowledge on cardiac energy metabolic pathways.

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“…The deregulation might be because of problems in the metabolic system or toxicological challenge exposure, and might even further provoke metabolic error. 71 , 72 …”

Section: Mitochondrial Dynamics In Cardiac Ischemiamentioning

confidence: 99%

<p>Targeting Cardiac Metabolic Pathways: A Role in Ischemic Management</p>

Yehualashet¹,

Belachew²,

Kifle³

et al. 2020

VHRM

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“…NADPH is involved in a variety of anabolic processes, such as the synthesis of lipids and nucleotides [ 6 , 7 ]. NADPH acts as a hydrogen donor in many biochemical reactions and is involved in the biotransformation of drugs, poisons, and some sex hormones [ 8 ]. Another important biological function of NADPH is to provide redox capacity for the antioxidant system, thus protecting cells against oxidative stress [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

Exogenous NADPH ameliorates myocardial ischemia–reperfusion injury in rats through activating AMPK/mTOR pathway

et al. 2019

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Our previous study shows that nicotinamide adenine dinucleotide phosphate (NADPH) plays an important role in protecting against cerebral ischemia injury. In this study we investigated whether NADPH exerted cardioprotection against myocardial ischemia/reperfusion (I/R) injury. To induce myocardial I/R injury, rats were subjected to ligation of the left anterior descending branch of coronary artery for 30 min followed by reperfusion for 2 h. At the onset of reperfusion, NADPH (4, 8, 16 mg· kg −1 · d −1 , iv) was administered to the rats. We found that NADPH concentrations in plasma and heart were significantly increased at 4 h after intravenous administration. Exogenous NADPH (8−16 mg/kg) significantly decreased myocardial infarct size and reduced serum levels of lactate dehydrogenase (LDH) and cardiac troponin I (cTn-I). Exogenous NADPH significantly decreased the apoptotic rate of cardiomyocytes, and reduced the cleavage of PARP and caspase-3. In addition, exogenous NADPH reduced mitochondrial vacuolation and increased mitochondrial membrane protein COXIV and TOM20, decreased BNIP3L and increased Bcl-2 to protect mitochondrial function. We conducted in vitro experiments in neonatal rat cardiomyocytes (NRCM) subjected to oxygen–glucose deprivation/restoration (OGD/R). Pretreatment with NADPH (60, 500 nM) significantly rescued the cell viability and inhibited OGD/R-induced apoptosis. Pretreatment with NADPH significantly increased the phosphorylation of AMPK and downregulated the phosphorylation of mTOR in OGD/R-treated NRCM. Compound C, an AMPK inhibitor, abolished NADPH-induced AMPK phosphorylation and cardioprotection in OGD/R-treated NRCM. In conclusion, exogenous NADPH exerts cardioprotection against myocardial I/R injury through the activation of AMPK/mTOR pathway and inhibiting mitochondrial damage and cardiomyocyte apoptosis. NADPH may be a potential candidate for the prevention and treatment of myocardial ischemic diseases.

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“…S9b †). Further considering that the intracellular level of NADH is signicantly higher than that of NADPH, 58,59 it can be seen that the signals we obtained came from the oxidation of intracellular NADH. Further converting the current signals to charge data (the corresponding charge statistics are shown as Fig.…”

Section: +mentioning

confidence: 75%