Table 2.
Summary of techniques and results of the discussed studies.
| Reference | Species | Technique | Biofluid/Tissue | Metabolites/Metabolism Discrimination |
|---|---|---|---|---|
| Andreadu et al., 2009 [50] | Wistar rats | NMR | Aqueous myocardial extracts | Increased levels of acetate and succinate, decreased levels of branched-chain amino acids |
| Andreadu et al., 2014 [51] | Wistar rats | NMR | Aqueous myocardial extracts | Perturbations of energy metabolism |
| Tan et al., 2011 [52] | ICR mice | GC–MS | Myocardial tissue | Increased levels of l-alanine, phosphate, glycine, succinate, malate, proline, threonic acid, glutamine, phenylalanine, dihydroxyacetonephosphate (DHAP), glycerol-3-phosphate (G-3-P), fructose, glucose, stearic acid, myo-inositol and cholesterol; decreased levels of lactate, β-hydroxybutyric acid, l-valine, isoleucine, threonine, citrate, linoleic acid, arachidonic acid |
| Cong et al., 2012 [53] | Sprague-Dawley rats | UPLC–TOF-MS | Urine | Metabolites involved in metabolic process related to myocardial energy metabolism: tricarboxylic acid cycle (citrate), glycolysis (lactate), pentose phosphate pathway (d-gluconate-1-phosphate) and amino acid metabolism (N-acetylglutamine and N-acetyl-dl-tryptophan) |
| Li et al., 2015 [54] | Wistar rats | UPLC–Q-TOF-MS | Plasma | l-carnitine, 19-hydroxydioxycortic acid, LPC (14:0) and LPC (20:2) |
| Schnackenberg et al., 2016 [55] | B6C3F1 mice | GC-MS, NMR | Heart tissue, Plasma | Myocardial specimens: altered levels of 18 amino acids and acetylornithine, kynurenine, putrescine and serotonin, decreased levels of 5 acylcarnitines. Plasma samples: altered levels of 16 amino acids and acetylornithine and hydroxyproline, increased levels of 16 acylcarnitines |
| Yin et al., 2016 [56] | Wistar rats | UPLC–Q-TOF-MS | Plasma | l-carnitine, proline, 19-hydroxydeoxycorticosterone, phuyoshingosine, cholic acid, LPC (14:0), LPC (18:3), LPC (16:1), LPE (18:2), LPC (22:5), LPC (22:6), linoleic acid, LPC (22:4), LPC (20:2), LPE (18:0), LPC (20:3) |
| Chaudhari et al., 2017 [57] | Human induced pluripotent stem cell-derived cardiomyocytes | NMR | Culture medium | Reduction in the utilisation of pyruvate and acetate, and accumulation of formate |
| QuanJun et al., 2017 [58] | BALB/c mice | NMR | Serum | DOX administration: increase in 5-hydroxylisine, 2-hydroxybutyrate, 2-oxoglutarate, 3-hydroxybutyrate decrease in glucose, glutamate, cysteine, acetone, methionine, asparate, isoleucine and glycylproline. DZR treatment: increase in lactate, 3-hydroxybutyrate, glutamate, alanine; decrease in glucose, trimethylamine N-oxide and carnosine levels |
| Jensen et al., 2017 [59] | FVB/N mice | GC–MS | Plasma and heart, skeletal muscle and liver tissues | Significant alterations in 11 metabolites, including markedly altered taurine/hypotaurine metabolism: glutamine, ethanolamine, stearamide, taurine, O-phosphocolamine, hypotaurine, myo-inosithol-2-phosphate, dehydroalanine, adenosine-5-monophosphate, glycerol-1-phosphate |
| Jensen et al., 2017 [60] | FVB/N mice | GC-MS | Serum and heart, skeletal muscle and liver tissues | Significantly lower heart and skeletal muscle levels of long chain omega-3 fatty acids docosahexaenoic acid (DHA), arachidonic acid (AA)/eicosapentaenoic acid (EPA) and increased serum O-phosphocholine phospholipid |
| Yoon et al., 2019 [61] | Human cardiomyocytes | NMR | Cardiomyocites | Decrease of acetate, glutamine, serine, uracil, glycerol; increase of glutamate, isoleucine, O-phosphocholine, taurine, myo-inositol, glutathione, sn-glycero-3-phosphocholine |
| Gramatyka et al., 2018 [62] | Human cardiomyocytes | HR-MAS NMR (High-Resolution Magic-Angle-Spinning Nuclear Magnetic Resonance) | Cardiomyocites | Lipids, threonine, glycine, glycerophosphocholine, choline, valine, isoleucine, glutamate; reduced glutathione and taurine metabolism |
UPLC–TOF/MS: Ultra-performance liquid chromatography–time-of-flight mass spectrometry; UPLC–QTOF/MS: Ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry; LPE: lysophosphatidylethanolamine.