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. Author manuscript; available in PMC: 2018 Jul 11.
Published in final edited form as: J Am Coll Cardiol. 2017 Jul 11;70(2):212–229. doi: 10.1016/j.jacc.2017.05.035

Figure 1. Mitochondrial ROS Generation in HF.

Figure 1

In HF, the regulation of mitochondrial ROS emission is controlled by ion handling and mechanical workload. Increased myocyte workload and dysregulation of calcium (Ca2+) and sodium (Na+) handling reduce mitochondrial Ca2+ accumulation, causing NADH and NADPH oxidation. NADPH depletion provokes H2O2 emission from mitochondria. ANT = adenine nucleotide translocator; ADP = adenosine diphosphate; ATP = adenosine triphosphate; ATPase = adenosine triphosphatase; GPX = glutathione peroxidase; GR = glutathione reductase; GSH/GSSG = reduced/oxidized glutathione; HF = heart failure; H2O2 = hydrogen peroxide; IDH = isocitrate dehydrogenase; IMM = inner mitochondrial membrane; MCU = mitochondrial calcium uniporter; NADH = nicotinamide adenine dinucleotide; NADPH = nicotinamide adenine dinucleotide phosphate; NCLX = mitochondrial sodium/calcium (and lithium) exchanger; NNT = nicotinamide nucleotide transhydrogenase; O2− = superoxide; OMM = outer mitochondrial membrane; PRX = peroxiredoxin; ROS = reactive oxygen species; RyR = ryanodine receptor; SERCA = sarcoplasmic reticulum calcium adenosine triphosphatase; TR = thioredoxin reductase; TRXr/o = reduced/oxidized thioredoxin.