代谢在生理性和病理性心室重构的研究进展
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摘要
代谢途径支持组织稳态和促进细胞表型改变,尤其是在消耗能量最大的心脏,底物不仅可以再生ATP用于心肌收缩,还可以维持细胞结构的生物合成反应。代谢途径也控制细胞内氧化还原状态,同时代谢中间产物和终产物可促进酶活性和基因表达的变化。越来越多的证据表明,在运动、妊娠、发育期间以及病理性应激中发生心脏代谢的变化是心室重构的原因。本文综述整合了不同形式心室重构的知识,以葡萄糖分解与合成代谢间的关系为基础,进一步阐述代谢如何调节心脏结构和功能。
The metabolic pathways support tissue homeostasis and promote cell phenotypic changes, especially in organs where the heart consumes the most energy. The substrate not only regenerates ATP for myocardial contraction, but also maintains the biosynthesis of cellular structures.Metabolic pathways also control intracellular redox states, metabolic intermediates, and end products, providing signals that promote changes in enzyme activity and gene expression. There is increasing evidence that changes in cardiac metabolism during exercise, pregnancy, developing and pathological stress are among the causes of ventricular remodeling. Disorders of catabolism and anabolism are becoming major causes of pathological ventricular remodeling. This review integrates knowledge of different forms of ventricular remodeling, based on the relationship between glucose breakdown and anabolism, and further illustrates how metabolism regulates cardiac structure and function.
The metabolic pathways support tissue homeostasis and promote cell phenotypic changes, especially in organs where the heart consumes the most energy. The substrate not only regenerates ATP for myocardial contraction, but also maintains the biosynthesis of cellular structures.Metabolic pathways also control intracellular redox states, metabolic intermediates, and end products, providing signals that promote changes in enzyme activity and gene expression. There is increasing evidence that changes in cardiac metabolism during exercise, pregnancy, developing and pathological stress are among the causes of ventricular remodeling. Disorders of catabolism and anabolism are becoming major causes of pathological ventricular remodeling. This review integrates knowledge of different forms of ventricular remodeling, based on the relationship between glucose breakdown and anabolism, and further illustrates how metabolism regulates cardiac structure and function.
引文
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[2] Doenst T,Nguyen T D,Abel E D.Cardiac metabolism in heart failure:implications beyond ATP production[J].Circulation Research,2013,113(6):709-24.
[3] Wang S C.The Study on the Academic Guidance System of Harvard University and Its Inspiration[J].Heilongjiang Researches on Higher Education,2016(2):89-91.
[4] Hew-Butler T,Verbalis J G,Noakes T D.Updated fluid recommendation:position statement from the International Marathon Medical Directors Association (IMMDA)[J].Clinical Journal of Sport Medicine Official Journal of the Canadian Academy of Sport Medicine,2006,16(4):283.
[5] Maillet M,van Berlo J H,Molkentin J D.Molecular basis of physiological heart growth:fundamental concepts and new players[J].Nature Reviews Molecular Cell Biology,2013,14(1):38-48.
[6] Souza L C,Jesse C R,Del F L,et al.Aging exacerbates cognitive and anxiety alterations induced by an intracerebroventricular injection of amyloid-β1-42 peptide in mice[J].Molecular & Cellular Neurosciences,2018,88:115-127.
[7] Panhuyzen-Goedkoop N M,Wellens H J,Piek J J.Early recognition of sudden cardiac arrest in athletes during sports activity[J].Netherlands Heart Journal,2018,26(1):1-5.
[8] Calvert J W,Elston M,Aragón J P,et al.Exercise Protects Against Myocardial Ischemia-Reperfusion injury via stimulation of β3-Adrenergic Receptors and Increased Nitric Oxide Signaling:Role of Nitrite and Nitrosothiols[J].Circulation Research,2011,108(12):1448-58.
[9] Platt C,Houstis N,Rosenzweig A.Using Exercise to Measure and Modify Cardiac Function[J].Cell Metabolism,2015,21(2):227.
[10] Guasch E,Mont L.Exercise,sex and atrial fibrillation:arrhythmogenesis beyond Y-chromosome?[J].Heart,2015,101(20):1607.
[11] Vega R B,Konhilas J P,Kelly D P,et al.Molecular Mechanisms Underlying Cardiac Adaptation to Exercise[J].Cell Metabolism,2017,25(5):1012.
[12] Yokokawa T,Sugano Y,Shimouchi A,et al.Exhaled Acetone Concentration Is Related to Hemodynamic Severity in Patients With Non-Ischemic Chronic Heart Failure[J].Circulation Journal Official Journal of the Japanese Circulation Society,2016,80(5):1178.
[13] Kanaroglou N,Farhat W A.Physiology of Minimally Invasive Surgery Versus Open Surgery[M].Springer London,2014:33-44.
[14] Smith D W,Fisher J A.Device to reduce SLOSH energy absorption and its damaging effects through the reduction of the flow of one or more outflow vessels of the cranium:us2016/0008004A1[P/OL].2016-01-14[2018-07-23].http:www.freepatentsonline.com/2016000804.pdf.
[15] Limon-Miranda S,Salazar-Enriquez D G,Muňiz J,et al.Pregnancy Differentially Regulates the Collagens Types Ⅰ and Ⅲ in Left Ventricle from Rat Heart[J].Biomed Research International,2014,2014(7):984785.
[16] Bett G C.Hormones and sex differences:changes in cardiac electrophysiology with pregnancy[J].Clinical Science,2016,130(10):747.
[17] Li J,Ruffenach G,Kararigas G,et al.Intralipid protects the heart in late pregnancy against ischemia/reperfusion injury via Caveolin2/STAT3/GSK-3β pathway[J].Journal of Molecular & Cellular Cardiology,2017,102:108-16.
[18] Chung E,Leinwand L A.Pregnancy as a cardiac stress model[J].Cardiovascular Research,2014,101(4):561-70.
[19] Xu H,Van D E,Johnson M,et al.Pregnancy mitigates cardiac pathology in a mouse model of left ventricular pressure overload[J].American Journal of Physiology Heart & Circulatory Physiology,2016,311(3):56.
[20] Shao M,Hepler C,Vishvanath L,et al.Fetal development of subcutaneous white adipose tissue is dependent on Zfp423[J].Molecular Metabolism,2017,6(1):111-24.
[21] Marcela S G,Cristina R M,Angel P G,et al.Chronological and morphological study of heart development in the rat[J].Anatomical Record Advances in Integrative Anatomy & Evolutionary Biology,2012,295(8):1267-90.
[22] Ritterhoff J,Tian R.Metabolism in cardiomyopathy:every substrate matters[J].Cardiovascular Research,2017,113(4):411-21.
[23] Neubauer S.The failing heart-an engine out of fuel[J].New England Journal of Medicine,2007,356(11):1140.
[24] Lee A P,Fang F,Jin C N,et al.Quantification of mitral valve morphology with three-dimensional echocardiography-can measurement lead to better management?[J].Circulation Journal,2014,78(5):1029-37.
[25] Bella J N,G?ring H H.Genetic epidemiology of left ventricular hypertrophy[J].American Journal of Cardiovascular Disease,2012,2(4):267-78.
[26] Coppiello G,Collantes M,Sirerolpiquer M S,et al.Meox2/Tcf15 Heterodimers Program the Heart Capillary Endothelium for Cardiac Fatty Acid Uptake[J].Circulation,2015,131(9):815.
[27] Nis S,Steen L,Martin H M,et al.Decreased mitochondrial oxidative phosphorylation capacity in the human heart with left ventricular systolic dysfunction[J].European Journal of Heart Failure,2013,15(2):150.
[28] Lopaschuk G D.Metabolic Modulators in Heart Disease:Past,Present,and Future[J].Canadian Journal of Cardiology,2016,33(7):838.
[29] Mori J,Basu R,Mclean B A,et al.Agonist-induced hypertrophy and diastolic dysfunction are associated with selective reduction in glucose oxidation:a metabolic contribution to heart failure with normal ejection fraction[J].Circulation Heart Failure,2012,5(4):493.
[30] Aubert G,Martin O J,Horton J L,et al.The Failing Heart Relies on Ketone Bodies as a Fuel[J].Circulation,2016,133(8):698-705.
[31] Sun H,Olson K C,Gao C,et al.Catabolic Defect of Branched-Chain Amino Acids Promotes Heart Failure[J].Circulation,2016,133(21):2038-49.