[1] “Heart Disease and Stroke Statistics—2019 Update: A Report From the American Heart Association,” Circulation, p. 473, doi: 10.1161/CIR.0000000000000659.
[2] G. Olivetti et al., “Apoptosis in the Failing Human Heart,” N. Engl. J. Med., vol. 336, no. 16, pp. 1131–1141, Apr. 1997, doi: 10.1056/NEJM199704173361603.
[3] Heinrich Taegtmeyer et al., “Assessing Cardiac Metabolism: A Scientific Statement From the American Heart Association,” Circ. Res., vol. 118, no. 10, pp. 1659–1701, May 2016, doi: 10.1161/RES.0000000000000097.
[4] Robert W. McGarrah, Scott B. Crown, Guo-Fang Zhang, Svati H. Shah, and Christopher B. Newgard, “Cardiovascular Metabolomics,” Circ. Res., vol. 122, no. 9, pp. 1238–1258, Apr. 2018, doi: 10.1161/CIRCRESAHA.117.311002.
[5] Yong Fan et al., “Comprehensive Metabolomic Characterization of Coronary Artery Diseases,” J. Am. Coll. Cardiol., vol. 68, no. 12, pp. 1281–1293, Sep. 2016, doi: 10.1016/j.jacc.2016.06.044.
[6] Brian E. Sansbury et al., “Metabolomic Analysis of Pressure-Overloaded and Infarcted Mouse Hearts,” Circ. Heart Fail., vol. 7, no. 4, pp. 634–642, Jul. 2014, doi: 10.1161/CIRCHEARTFAILURE.114.001151.
[7] X. Liang, L. Zhang, S. K. Natarajan, and D. F. Becker, “Proline Mechanisms of Stress Survival,” Antioxid. Redox Signal., vol. 19, no. 9, pp. 998–1011, Sep. 2013, doi: 10.1089/ars.2012.5074.
[8] S. K. Natarajan et al., “Proline dehydrogenase is essential for proline protection against hydrogen peroxide-induced cell death,” Free Radic. Biol. Med., vol. 53, no. 5, pp. 1181–1191, Sep. 2012, doi: 10.1016/j.freeradbiomed.2012.07.002.
[9] C. D’Aniello, E. J. Patriarca, J. M. Phang, and G. Minchiotti, “Proline Metabolism in Tumor Growth and Metastatic Progression,” Front. Oncol., vol. 10, p. 776, May 2020, doi: 10.3389/fonc.2020.00776.
[10] Y. Fichman, S. Y. Gerdes, H. Kovács, L. Szabados, A. Zilberstein, and L. N. Csonka, “Evolution of proline biosynthesis: enzymology, bioinformatics, genetics, and transcriptional regulation: Proline biosynthesis,” Biol. Rev., vol. 90, no. 4, pp. 1065–1099, Nov. 2015, doi: 10.1111/brv.12146.
[11] Kai-Chien Yang et al., “Deep RNA Sequencing Reveals Dynamic Regulation of Myocardial Noncoding RNAs in Failing Human Heart and Remodeling With Mechanical Circulatory Support,” Circulation, vol. 129, no. 9, pp. 1009–1021, Mar. 2014, doi: 10.1161/CIRCULATIONAHA.113.003863.
[12] J. O. Kim et al., “A novel system-level approach using RNA-sequencing data identifies miR-30-5p and miR-142a-5p as key regulators of apoptosis in myocardial infarction,” Sci. Rep., vol. 8, no. 1, p. 14638, Dec. 2018, doi: 10.1038/s41598-018-33020-x.
[13] “Comprehensive Metabolomic Characterization of Coronary Artery Diseasesmmc1.pdf.” .
[14] W. Wang et al., “Defective branched chain amino acid catabolism contributes to cardiac dysfunction and remodeling following myocardial infarction,” Am. J. Physiol.-Heart Circ. Physiol., vol. 311, no. 5, pp. H1160–H1169, Nov. 2016, doi: 10.1152/ajpheart.00114.2016.
[15] H. Sun et al., “Catabolic Defect of Branched-Chain Amino Acids Promotes Heart Failure,” Circulation, vol. 133, no. 21, pp. 2038–2049, May 2016, doi: 10.1161/CIRCULATIONAHA.115.020226.
[16] “Chong 等。 - 2018 - MetaboAnalyst 4.0 towards more transparent and in.pdf.” .
[17] C. J. Zuurbier et al., “Cardiac metabolism as a driver and therapeutic target of myocardial infarction,” J. Cell. Mol. Med., vol. 24, no. 11, pp. 5937–5954, Jun. 2020, doi: 10.1111/jcmm.15180.
[18] E. E. Egom, M. A. Mamas, and A. L. Clark, “The potential role of sphingolipid-mediated cell signaling in the interaction between hyperglycemia, acute myocardial infarction and heart failure,” Expert Opin. Ther. Targets, vol. 16, no. 8, pp. 791–800, Aug. 2012, doi: 10.1517/14728222.2012.699043.
[19] E. E. Egom et al., “Serum sphingolipids level as a novel potential marker for early detection of human myocardial ischaemic injury,” Front. Physiol., vol. 4, 2013, doi: 10.3389/fphys.2013.00130.
[20] E. E. A. Egom et al., “Activation of Pak1/Akt/eNOS signaling following sphingosine-1-phosphate release as part of a mechanism protecting cardiomyocytes against ischemic cell injury,” Am. J. Physiol.-Heart Circ. Physiol., vol. 301, no. 4, pp. H1487–H1495, Oct. 2011, doi: 10.1152/ajpheart.01003.2010.
[21] Y. Hadas et al., “Altering Sphingolipid Metabolism Attenuates Cell Death and Inflammatory Response After Myocardial Infarction,” Circulation, vol. 141, no. 11, pp. 916–930, Mar. 2020, doi: 10.1161/CIRCULATIONAHA.119.041882.
[22] P. C. Calder, “Very long-chain n -3 fatty acids and human health: fact, fiction and the future,” Proc. Nutr. Soc., vol. 77, no. 1, pp. 52–72, Feb. 2018, doi: 10.1017/S0029665117003950.
[23] C. Bilato, “n-3 Fatty acids and cardiovascular disease: the story is not over yet,” Aging Clin. Exp. Res., vol. 25, no. 4, pp. 357–363, Aug. 2013, doi: 10.1007/s40520-013-0077-y.
[24] A. W. Qureshi et al., “Ageing enhances the shedding of splenocyte microvesicles with endothelial pro-senescent effect that is prevented by a short-term intake of omega-3 PUFA EPA:DHA 6:1,” Biochem. Pharmacol., vol. 173, p. 113734, Mar. 2020, doi: 10.1016/j.bcp.2019.113734.
[25] E. B. Rimm et al., “Seafood Long-Chain n-3 Polyunsaturated Fatty Acids and Cardiovascular Disease: A Science Advisory From the American Heart Association,” Circulation, vol. 138, no. 1, Jul. 2018, doi: 10.1161/CIR.0000000000000574.
[26] P. A. Bottomley, K. C. Wu, G. Gerstenblith, S. P. Schulman, A. Steinberg, and R. G. Weiss, “Reduced Myocardial Creatine Kinase Flux in Human Myocardial Infarction: An In Vivo Phosphorus Magnetic Resonance Spectroscopy Study,” Circulation, vol. 119, no. 14, pp. 1918–1924, Apr. 2009, doi: 10.1161/CIRCULATIONAHA.108.823187.
[27] M. Balestrino, M. Sarocchi, E. Adriano, and P. Spallarossa, “Potential of creatine or phosphocreatine supplementation in cerebrovascular disease and in ischemic heart disease,” Amino Acids, vol. 48, no. 8, pp. 1955–1967, Aug. 2016, doi: 10.1007/s00726-016-2173-8.
[28] N. Krishnan, M. B. Dickman, and D. F. Becker, “Proline modulates the intracellular redox environment and protects mammalian cells against oxidative stress,” Free Radic. Biol. Med., vol. 44, no. 4, pp. 671–681, Feb. 2008, doi: 10.1016/j.freeradbiomed.2007.10.054.
[29] E. R. S. Torres et al., “Integrated Metabolomics-DNA Methylation Analysis Reveals Significant Long-Term Tissue-Dependent Directional Alterations in Aminoacyl-tRNA Biosynthesis in the Left Ventricle of the Heart and Hippocampus Following Proton Irradiation,” Front. Mol. Biosci., vol. 6, p. 77, Sep. 2019, doi: 10.3389/fmolb.2019.00077.
[30] Z.-Y. Zhang et al., “Diastolic left ventricular function in relation to circulating metabolic biomarkers in a population study,” Eur. J. Prev. Cardiol., vol. 26, no. 1, pp. 22–32, Jan. 2019, doi: 10.1177/2047487318797395.
[31] E. A. Hausner, S. A. Elmore, and X. Yang, “Overview of the Components of Cardiac Metabolism,” Drug Metab. Dispos., vol. 47, no. 6, pp. 673–688, Jun. 2019, doi: 10.1124/dmd.119.086611.
[32] H. Bai et al., “Proteomic and metabolomic characterization of cardiac tissue in acute myocardial ischemia injury rats,” PLOS ONE, vol. 15, no. 5, p. e0231797, May 2020, doi: 10.1371/journal.pone.0231797.