Abstract

Left ventricular hypertrophy (LVH) is a strong predictor of adverse cardiovascular outcomes. It is the result of complex mechanisms that include not only an increase in protein synthesis and cell size but also proliferating cardiac progenitor cells and the influx of bone marrow-derived cells developing into cardiomyocytes. Stem and progenitor cells are known to contribute to the renewal of adult mammalian cardiomyocytes in case of myocardial injury or pressure and volume overload. They are activated in LVH and play a regulatory role in myocardial repair. They have high proliferative potential and secrete numerous cytokines, growth factors, and microRNAs that play important roles in cell differentiation, cardiac remodeling, and neovascularization. They are mobilized in response to either mechanical or chemical stimuli, hormones, or pharmacologic agents. Another important source of progenitor cells is the epicardial layer. It appears that precursor cells migrate from the epicardium to the myocardium in order to interact with myocardial cells. In addition, migratory cells participate in the formation of almost all cardiac structures in myocardial hypertrophy. Although the pathophysiological mechanisms are still obscure and further studies are required, their properties may open the door to regenerative cell therapy for the prevention of adverse remodeling.

Highlights

  • Left ventricular hypertrophy (LVH) is a strong predictor of adverse cardiovascular outcomes and an important risk factor for sudden death and heart failure [1]

  • LVH is the result of an increase in protein synthesis and cell size and of proliferating cardiac progenitor cells and the influx of bone marrow-derived cells developing into cardiomyocytes [3,4,5,6]

  • It has been shown that an increase in preload results in the mobilization of progenitor cells from the bone marrow for use in neovascularization, which plays a pivotal role in cardiac hypertrophy [32]

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Summary

Introduction

Left ventricular hypertrophy (LVH) is a strong predictor of adverse cardiovascular outcomes and an important risk factor for sudden death and heart failure [1]. LVH is a complex and multifactorial condition whose pathogenesis may include many different genetic and signaling pathways [2]. It involves a process of adaptive remodeling, which is usually a compensatory mechanism in response to increased hemodynamic load. This mechanism is beneficial in most cases [2]. It is characterized by structural changes, mainly in the form of myocardial fibrosis, that lead to diastolic dysfunction and diminished contractility

Physiological and Pathological Myocardial Hypertrophy
Myocardial Regeneration and Stem Cells
Description and Location of CSCs
Left Ventricular Hypertrophy in Aortic Diseases
Left Ventricular Hypertrophy in Arterial Hypertension
Stem Cells and Hypertrophic Cardiomyopathy
Stem Cells and New Perspectives
Findings
10. Conclusion
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