Physiological and pathological cardiac hypertrophy

被引:707
作者
Shimizu, Ippei [1 ,2 ]
Minamino, Tohru [1 ]
机构
[1] Niigata Univ, Grad Sch Med & Dent Sci, Dept Cardiovasc Biol & Med, Niigata 9518510, Japan
[2] Niigata Univ, Div Mol Aging & Cell Biol, Grad Sch Med & Dent Sci, Niigata 9518510, Japan
关键词
Cardiac hypertrophy; Heart failure; Angiogenesis; Akt; Autophagy; Inflammation; Epigenetic modification; MicroRNA; Metabolism; GROWTH-FACTOR-I; CA2+/CALMODULIN-DEPENDENT PROTEIN-KINASE; LEFT-VENTRICULAR HYPERTROPHY; FATTY-ACID OXIDATION; PRESSURE-OVERLOAD HYPERTROPHY; SKELETAL-MUSCLE HYPERTROPHY; MEF2 TRANSCRIPTION FACTOR; HEART-FAILURE; THYROID-HORMONE; ANGIOTENSIN-II;
D O I
10.1016/j.yjmcc.2016.06.001
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
The heart must continuously pump blood to supply the body with oxygen and nutrients. To maintain the high energy consumption required by this role, the heart is equipped with multiple complex biological systems that allow adaptation to changes of systemic demand. The processes of growth (hypertrophy), angiogenesis, and metabolic plasticity are critically involved in maintenance of cardiac homeostasis. Cardiac hypertrophy is classified as physiological when it is associated with normal cardiac function or as pathological when associated with cardiac dysfunction. Physiological hypertrophy of the heart occurs in response to normal growth of children or during pregnancy, as well as in athletes. In contrast, pathological hypertrophy is induced by factors such as prolonged and abnormal hemodynamic stress, due to hypertension, myocardial infarction etc. Pathological hypertrophy is associated with fibrosis, capillary rarefaction, increased production of pro-inflammatory cytokines, and cellular dysfunction (impairment of signaling, suppression of autophagy, and abnormal cardiomyocyte/non-cardiomyocyte interactions), as well as undesirable epigenetic changes, with these complex responses leading to maladaptive cardiac remodeling and heart failure. This review describes the key molecules and cellular responses involved in physiological/pathological cardiac hypertrophy. (C) 2016 Elsevier Ltd. All rights reserved.
引用
收藏
页码:245 / 262
页数:18
相关论文
共 286 条
[1]
Cardiac hypertrophy with preserved contractile function after selective deletion of GLUT4 from the heart [J].
Abel, ED ;
Kaulbach, HC ;
Tian, R ;
Hopkins, JCA ;
Duffy, J ;
Doetschman, T ;
Minnemann, T ;
Boers, ME ;
Hadro, E ;
Oberste-Berghaus, C ;
Quist, W ;
Lowell, BB ;
Ingwall, JS ;
Kahn, BB .
JOURNAL OF CLINICAL INVESTIGATION, 1999, 104 (12) :1703-1714
[2]
Akt1/protein kinase Bα is critical for ischemic and VEGF-mediated angiogenesis [J].
Ackah, E ;
Yu, J ;
Zoellner, S ;
Iwakiri, Y ;
Skurk, C ;
Shibata, R ;
Ouchi, N ;
Easton, RM ;
Galasso, G ;
Birnbaum, MJ ;
Walsh, K ;
Sessa, WC .
JOURNAL OF CLINICAL INVESTIGATION, 2005, 115 (08) :2119-2127
[3]
Ca2+/calmodulin-dependent protein kinase modulates cardiac ryanodine receptor phosphorylation and sarcoplasmic reticulum Ca2+ leak in heart failure [J].
Ai, X ;
Curran, JW ;
Shannon, TR ;
Bers, DM ;
Pogwizd, SM .
CIRCULATION RESEARCH, 2005, 97 (12) :1314-1322
[4]
Sirt1 regulates aging and resistance to oxidative stress in the heart [J].
Alcendor, Ralph R. ;
Gao, Shumin ;
Zhai, Peiyong ;
Zablocki, Daniela ;
Holle, Eric ;
Yu, Xianzhong ;
Tian, Bin ;
Wagner, Thomas ;
Vatner, Stephen F. ;
Sadoshima, Junichi .
CIRCULATION RESEARCH, 2007, 100 (10) :1512-1521
[5]
Myocardial infarction in rats causes partial impairment in insulin response associated with reduced fatty acid oxidation and mitochondrial gene expression [J].
Amorim, Paulo A. ;
Nguyen, T. Dung ;
Shingu, Yasushige ;
Schwarzer, Michael ;
Mohr, Friedrich W. ;
Schrepper, Andrea ;
Doenst, Torsten .
JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY, 2010, 140 (05) :1160-1167
[6]
Titin-based tension in the cardiac sarcomere: Molecular origin and physiological adaptations [J].
Anderson, Brian R. ;
Granzier, Henk L. .
PROGRESS IN BIOPHYSICS & MOLECULAR BIOLOGY, 2012, 110 (2-3) :204-217
[7]
ALTERNATIVE PATHWAY OF INSULIN SIGNALING IN MICE WITH TARGETED DISRUPTION OF THE IRS-1 GENE [J].
ARAKI, E ;
LIPES, MA ;
PATTI, ME ;
BRUNING, JC ;
HAAG, B ;
JOHNSON, RS ;
KAHN, CR .
NATURE, 1994, 372 (6502) :186-190
[8]
Cardiac-specific overexpression of diacylglycerol kinase ξ prevents Gq protein-coupled receptor agonist-induced cardiac hypertrophy in transgenic mice [J].
Arimoto, T ;
Takeishi, Y ;
Takahashi, H ;
Shishido, T ;
Niizeki, T ;
Koyama, Y ;
Shiga, R ;
Nozaki, N ;
Nakajima, O ;
Nishimaru, K ;
Abe, J ;
Walsh, RA ;
Goto, K ;
Kubota, I .
CIRCULATION, 2006, 113 (01) :60-66
[9]
Metabolic mechanisms in heart failure [J].
Ashrafian, Houman ;
Frenneaux, Michael P. ;
Opie, Lionel H. .
CIRCULATION, 2007, 116 (04) :434-448
[10]
Unrestrained p38 MAPK Activation in Dusp1/4 Double-Null Mice Induces Cardiomyopathy [J].
Auger-Messier, Mannix ;
Accornero, Federica ;
Goonasekera, Sanjeewa A. ;
Bueno, Orlando F. ;
Lorenz, John N. ;
van Berlo, Jop H. ;
Willette, Robert N. ;
Molkentin, Jeffery D. .
CIRCULATION RESEARCH, 2013, 112 (01) :48-+