Molecular mechanisms in evolutionary cardiology failure

Integration of the relevant evolutionary paradigm in cardiology has not yet been fully achieved: In the past, heart failure (HF) was mainly ascribed to infections, and the origins of cardiac hypertrophy (CH) were regarded as mechanical. Recent changes in lifestyle have both reduced the incidence of infections and increased lifespan, and HF is now seen as a complex disease—one that is still caused by mechanical disorder, but also associated with ischemia and senescence. The long‐held view that CH serves to restore myocardial economy back to normal is still valid. The adaptive process is characterized by a quantitative and a qualitative fetal gene reprogramming, which is now being confirmed by recent advances in microRNA research. It underscores the fact CH is the physiologic reaction of the heart to a pathologic stimulus. The goal for therapy is economic, not inotropic. Another major issue is myocardial fibrosis, a major determinant of diastolic function and arrhythmias. Recent changes in lifestyle have crucially modified the context in which HF occurs.

[1]  W. Rottbauer,et al.  MicroRNA-21 contributes to myocardial disease by stimulating MAP kinase signalling in fibroblasts , 2008, Nature.

[2]  W. Dunn,et al.  Genomics in cardiac metabolism. , 2008, Cardiovascular research.

[3]  S. Petrungaro,et al.  c-Flip overexpression reduces cardiac hypertrophy in response to pressure overload , 2008, Journal of hypertension.

[4]  B. Swynghedauw,et al.  Is cardiac hypertrophy a required compensatory mechanism in pressure-overloaded heart? , 2008, Journal of hypertension.

[5]  M. Gerstein,et al.  What is a gene, post-ENCODE? History and updated definition. , 2007, Genome research.

[6]  M. Lynch.  The frailty of adaptive hypotheses for the origins of organismal complexity , 2007, Proceedings of the National Academy of Sciences.

[7]  Thomas Thum,et al.  MicroRNAs in the Human Heart: A Clue to Fetal Gene Reprogramming in Heart Failure , 2007, Circulation.

[8]  G. Lanfranchi,et al.  Differential gene expression profiling in genetic and multifactorial cardiovascular diseases. , 2006, Journal of molecular and cellular cardiology.

[9]  M. Zaugg,et al.  Integration of calcium with the signaling network in cardiac myocytes. , 2006, Journal of molecular and cellular cardiology.

[10]  B. Swynghedauw.  Phenotypic plasticity of adult myocardium: molecular mechanisms , 2006, Journal of Experimental Biology.

[11]  B. Swynghedauw,et al.  From molecular to modular cardiology. How to interpret the millions of data that came out from large scale analysis of gene expression? , 2006, Archives des maladies du coeur et des vaisseaux.

[12]  R. Irizarry,et al.  Gene expression analysis of ischemic and nonischemic cardiomyopathy: shared and distinct genes in the development of heart failure. , 2005, Physiological genomics.

[13]  Despina Sanoudou,et al.  Array lessons from the heart: focus on the genome and transcriptome of cardiomyopathies. , 2005, Physiological genomics.

[14]  D. Irwin,et al.  The role of phenotypic plasticity in driving genetic evolution , 2003, Proceedings of the Royal Society of London. Series B: Biological Sciences.

[15]  I. Komuro,et al.  Roles of cardiac transcription factors in cardiac hypertrophy. , 2003, Circulation research.

[16]  E. Lakatta,et al.  Sex- and age-dependent human transcriptome variability: Implications for chronic heart failure , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[17]  Paul D Allen,et al.  Global gene expression profiling of end-stage dilated cardiomyopathy using a human cardiovascular-based cDNA microarray. , 2002, The American journal of pathology.

[18]  Greg Gibson and Spencer V. Muse,et al.  A Primer of Genome Science , 2001 .

[19]  G. Buckberg,et al.  The structure and function of the helical heart and its buttress wrapping. V. Anatomic and physiologic considerations in the healthy and failing heart. , 2001, Seminars in thoracic and cardiovascular surgery.

[20]  J. DiMaio,et al.  Adaptive Mechanisms That Preserve Cardiac Function in Mice Without Myoglobin , 2001, Circulation research.

[21]  E. Lander,et al.  Remodeling of yeast genome expression in response to environmental changes. , 2001, Molecular biology of the cell.

[22]  C. Baillard,et al.  Biology of hypertensive cardiopathy , 2000, Current opinion in cardiology.

[23]  G. Shipley,et al.  Unloaded heart in vivo replicates fetal gene expression of cardiac hypertrophy , 1998, Nature Medicine.

[24]  Jeffrey Robbins,et al.  A Calcineurin-Dependent Transcriptional Pathway for Cardiac Hypertrophy , 1998, Cell.

[25]  F. Boucher,et al.  Effects of sustained low-flow ischemia on myocardial function and calcium-regulating proteins in adult and senescent rat hearts. , 1998, Cardiovascular research.

[26]  C. Delcayre,et al.  Myocardial Production of Aldosterone and Corticosterone in the Rat , 1998, The Journal of Biological Chemistry.

[27]  A. Wiley.  Why We Get Sick: The New Science of Darwinian Medicine , 1997 .

[28]  C. Delcayre,et al.  Biological determinants of aldosterone-induced cardiac fibrosis in rats. , 1995, Hypertension.

[29]  B. Swynghedauw.  Developmental and functional adaptation of contractile proteins in cardiac and skeletal muscles. , 1986, Physiological reviews.

[30]  B. Swynghedauw,et al.  Myosin isoenzyme redistribution in chronic heart overload , 1979, Nature.

[31]  J. van der Stok,et al.  Metabolic and genetic regulation of cardiac energy substrate preference. , 2007, Comparative biochemistry and physiology. Part A, Molecular & integrative physiology.

[32]  R. Tunin,et al.  Transcriptomic profiling of the canine tachycardia-induced heart failure model: global comparison to human and murine heart failure. , 2006, Journal of molecular and cellular cardiology.

[33]  H. Witt,et al.  Microarray analysis to evaluate different animal models for human heart failure. , 2006, Journal of molecular and cellular cardiology.

[34]  J. Magovern,et al.  Molecular dynamics of the compensatory response to myocardial infarct. , 2005, Journal of molecular and cellular cardiology.

[35]  N. Le Meur,et al.  Gene expression profiling in human cardiovascular disease , 2005, Clinical chemistry and laboratory medicine.

[36]  Luigi Fratta,et al.  Melusin, a muscle-specific integrin β1–interacting protein, is required to prevent cardiac failure in response to chronic pressure overload , 2003, Nature Medicine.

[37]  J. Haerting,et al.  Gene-expression signatures in breast cancer. , 2003, The New England journal of medicine.

[38]  W. Koch,et al.  Genetic Alterations That Inhibit In Vivo Pressure-Overload Hypertrophy Prevent Cardiac Dysfunction Despite Increased Wall Stress , 2002, Circulation.

[39]  B. Swynghedauw,et al.  Molecular mechanisms of myocardial remodeling. , 1999, Physiological reviews.

[40]  A. Carayon,et al.  , Brigitte Angiotensin II Receptor Blockade and Role in Cardiac Fibrosis Activation of Cardiac Aldosterone Production in Rat Myocardial Infarction : Effect of , 1999 .

[41]  W. Colucci.  Molecular Mechanisms of Myocardial Remodeling , 1999 .

[42]  G. Richards.  Why we get sick: The new science of Darwinian medicine , 1996 .

[43]  J. Bremerich,et al.  Regulation of β-adrenergic receptors in acute myocardial ischemia: subtype-selective increase of mRNA specific for β1-adrenergic receptors , 1995 .