The effective management of Cardiac remodeling(CR), remains a major challenge. Heart failure remains the leading cause of death in industrialized countries. Yet, despite the enormity of the problem, effective therapeutic interventions remain elusive. In fact, several initially promising agents were found to decrease mortality in patients recovering from myocardial infarction. Cardiac remodeling is defined as molecular and interstitial changes, manifested clinically by changes in size, mass , geometry and function of the heart in response to certain aggression. Initially, ventricular remodeling aims to maintain stable cardiac function in situations of aggression. Chronically, however, with the continuity and/or progression of the process of progressive ventricular dysfunction and death occurs. Myocardial infarction and/or acute ischemia provoke profound changes in the properties of cardiac muscle. The response of the heart to sustained load increases, as in hypertension and aortic stenosis, results in an increase in muscle mass in overloaded chamber. Mechanical overload and activation of circulating and tissue neurohormonal systems produce a number of cellular mediators: angiotensin II, endothelin-1, norepinephrine, aldosterone, cytokines (tumor necrosis factor alpha and interleukins) and release calcium which acts as intracellular marker. The activation of cellular mediators involved in CR can be primary or caused by myocardial stretch. In pressure overload, mechanical overload cellular mediators result in left ventricular hypertrophy, interstitial changes involving fibroblast proliferation, collagen accumulation and wall hypertrophy of intramyocardial coronary vessels. It is the purpose of this Research Topic to the evaluate the relationship between aggressive factors determinants of cardiac remodeling and changes properties of cardiac muscle. Authors are welcome to submit computational models, clinical, translational, or experimental research articles, reviews and hypotheses that address this topic. Studies are also welcome that focus on molecular mechanisms that deal with conditioning effects as such mechanisms are probably most important for our understanding of physiological behaviour of tissues during brief periods of ischemia that may occur occasionally, but also likely candidates to develop novel protective strategies in medical procedures.
This Research Topic welcomes review articles related to the field of cardiac remodeling.
Example topics of interest include:
1. Geometric changes of the left ventricle
2. Myocyte hypertrophy
3. Interstitial and perivascular fibrosis
4. Blood vessels and perivascular fibrosis
5. Defects in the coupling
6. Changes of b-adrenergic pathway
7. Changes in contractile proteins
8. Cell death (necrosis and apoptosis)
9. Cardiac Remodeling after Myocardial Infarction
10. Cardiac Remodeling in Hypertension
11. Cardiac remodeling in metabolic syndrome
12. Cardiac Remodeling in Heart Failure
13. Cardiac Remodeling in ischemia
15. Cardiac remodeling mediated by inflammatory factors
16. Cardiac Remodeling in ventricular dysfunction
17. Cardiac Remodeling and Endothelial Function
18. Cardiac Remodeling and exercise
19. Cardiac Remodeling in valve diseases
The effective management of Cardiac remodeling(CR), remains a major challenge. Heart failure remains the leading cause of death in industrialized countries. Yet, despite the enormity of the problem, effective therapeutic interventions remain elusive. In fact, several initially promising agents were found to decrease mortality in patients recovering from myocardial infarction. Cardiac remodeling is defined as molecular and interstitial changes, manifested clinically by changes in size, mass , geometry and function of the heart in response to certain aggression. Initially, ventricular remodeling aims to maintain stable cardiac function in situations of aggression. Chronically, however, with the continuity and/or progression of the process of progressive ventricular dysfunction and death occurs. Myocardial infarction and/or acute ischemia provoke profound changes in the properties of cardiac muscle. The response of the heart to sustained load increases, as in hypertension and aortic stenosis, results in an increase in muscle mass in overloaded chamber. Mechanical overload and activation of circulating and tissue neurohormonal systems produce a number of cellular mediators: angiotensin II, endothelin-1, norepinephrine, aldosterone, cytokines (tumor necrosis factor alpha and interleukins) and release calcium which acts as intracellular marker. The activation of cellular mediators involved in CR can be primary or caused by myocardial stretch. In pressure overload, mechanical overload cellular mediators result in left ventricular hypertrophy, interstitial changes involving fibroblast proliferation, collagen accumulation and wall hypertrophy of intramyocardial coronary vessels. It is the purpose of this Research Topic to the evaluate the relationship between aggressive factors determinants of cardiac remodeling and changes properties of cardiac muscle. Authors are welcome to submit computational models, clinical, translational, or experimental research articles, reviews and hypotheses that address this topic. Studies are also welcome that focus on molecular mechanisms that deal with conditioning effects as such mechanisms are probably most important for our understanding of physiological behaviour of tissues during brief periods of ischemia that may occur occasionally, but also likely candidates to develop novel protective strategies in medical procedures.
This Research Topic welcomes review articles related to the field of cardiac remodeling.
Example topics of interest include:
1. Geometric changes of the left ventricle
2. Myocyte hypertrophy
3. Interstitial and perivascular fibrosis
4. Blood vessels and perivascular fibrosis
5. Defects in the coupling
6. Changes of b-adrenergic pathway
7. Changes in contractile proteins
8. Cell death (necrosis and apoptosis)
9. Cardiac Remodeling after Myocardial Infarction
10. Cardiac Remodeling in Hypertension
11. Cardiac remodeling in metabolic syndrome
12. Cardiac Remodeling in Heart Failure
13. Cardiac Remodeling in ischemia
15. Cardiac remodeling mediated by inflammatory factors
16. Cardiac Remodeling in ventricular dysfunction
17. Cardiac Remodeling and Endothelial Function
18. Cardiac Remodeling and exercise
19. Cardiac Remodeling in valve diseases
