Pathological Left Ventricular Hypertrophy and Stem Cells: Current Evidence and New Perspectives

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.

The long noncoding RNA Chaer defines an epigenetic checkpoint in cardiac hypertrophy

“…Although our study focuses on cell-autonomous effect of Chaer on cardiomyocyte hypertrophy, the cardiac effect of Chaer expression may also involve other cellular process in non-myocyte cardiac cells. It is intriguing that FISH assay detected significant signal of Chaer within the mouse epicardium where potential progenitor cells for endothelium and fibroblasts have been reported to reside 54 , and Chaer KO significantly reduced TAC induced cardiac fibrosis. It is also interesting to observe that a significant number of cell cycle genes are regulated by Chaer .…”

CD38 promotes angiotensin II‐induced cardiac hypertrophy

“…Many factors could induce ventricular hypertrophy, such as Ang-II, ET-1, catecholamines, growth factors and TNF-a [30]. Among them, Ang-II is commonly used for induction of hypertrophic models, as it can potently induce pressure overload, which leads to an increase in wall thickness and concentric hypertrophy of the left ventricle as a compensatory mechanism to maintain the ventricular EF under conditions of increased peripheral resistance [31]. In the present study, we investigated the role of CD38 in the development of Ang-II-induced cardiac hypertrophy.…”

Remote transplantation of human adipose-derived stem cells induces regression of cardiac hypertrophy by regulating the macrophage polarization in spontaneously hypertensive rats

“…However, the migration ability of transplanted cells onto the heart was not addressed. Experimental studies have shown that an increase in preload results in the mobilization of progenitor cells from the bone marrow and migration into the heart, which plays an important role in cardiac hypertrophy [51]. Thus, we can not exclude the possibility of stem cells from the bone marrow in modulating ventricular hypertrophy.…”