Adverse Cardiac Remodeling: Phosphoinositide 3-Kinase, Another Unique Factor in a Multifactorial Condition
Left ventricular remodeling has originally been defined as enlargement due to "alterations in the topography of both the infarcted and noninfarcted regions of the ventricle" 1. Similar remodeling processes appear to follow other types of stress like pressure overload (aortic constriction). In contrast, physiologic hypertrophy represents the response of the healthy heart to exercise. Three decades of research have added comprehensive information beyond the organ level. Wound healing of the infarcted zone has become its own field of research2 and the role of inflammatory cells has been stressed recently3. Remodeling of various myocardial cell types includes myocyte concentric and eccentric hypertrophy, slippage, accumulation of interstitial tissue and rarefication of coronary vasculature in the non-infarcted myocardium4-6. Early observations on molecular changes include a shift of myocardial proteins and enzymes towards an embryonic pattern and a loss of cardiac energy reserve7. Changes of proteins result in impairment of excitation-contraction coupling and apoptosis8. More recently, a crucial role of microRNA in regulation of these and many other processes has been suggested9.
- Received September 16, 2012.
- Accepted September 19, 2012.
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