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Review
. 2010 Aug 31;122(9):928-37.
doi: 10.1161/CIRCULATIONAHA.108.847731.

Cell communications in the heart

Daniela Tirziu  1 , Frank J Giordano, Michael Simons
Affiliations
Review

Cell communications in the heart

Daniela Tirziu et al. Circulation. .
No abstract available

PubMed Disclaimer

Conflict of interest statement

Conflict of interest: None

Figures

Figure 1
Figure 1
Schematic representation of cell-cell communication modalities in the heart. Types of cell-cell cross-talk and their mediators. Abbreviations are the same as in the text.
Figure 2
Figure 2
Myocardial hypertrophy as result of cardiomyocyte – endothelium and endothelium – cardiomyocyte crosstalk. Hypertrophic programs can be activated by a direct myocyte stimulation such as pressure or volume overload (left side) or by an expansion of the cardiac vascular mass (right side). Myocyte-driven hypertrophic response includes production of angiogenic growth factors and other myocyte-derived molecules capable of stimulating endothelial expansion (myokines). The angiogenic response is crucial for normal function of the hypertrophic heart and its failure or imbalance in the extent of hypertrophic and angiogenic responses, leads to progressive deterioration of myocardial function and heart failure. On the other hand, increase in the endothelial cell mass in the normal heart can activate myocardial hypertrophy even in the absence of physical stimuli by secretion of nitric oxide, neuregulin (NRG-1) and putative “endokines” (endothelium-derived molecules capable of affecting myocytes). The excess of NO may result in heart failure due to its negative ionotropic properties
Figure 3
Figure 3
Cellular crosstalk paradigms in the heart. A number of local and long-distance cell-cell communications contribute to maintenance of normal cardiac homeostasis and to responses to hypertrophic stimuli. These include paracrine/autocrine and endocrine signals, direct cell-cell contacts via gap junction, and cell- matrix interactions between cells of the coronary vasculature, cardiomyocytes, fibroblasts and probably other cell types, including tissue-resident stem cells. Perturbations in the balance of this network during sustained hemodynamic stress can lead to a variety of pathological sequelae, including heart failure due to inadequate vascular compensation for myocyte hypertrophy, and the development of cardiac fibrosis as a consequence of fibroblast proliferation and remodeling of the extracellular matrix. formula image Growth factors (e.g. IGF, FGF, HB-EGF, PDGF, HGF, VEGF, etc.); formula image Stress enhancers (e.g. AngII, ET-1, etc.); formula image Endothelium signals (e.g. NO, NRG-1, apelin, angiopoientin-1, prostacyclin, etc.); formula image SMC (e.g. VEGF, angiopoientin, etc); formula image Cardiomyocyte signals (e.g. Fslt-1, VEGF, FGF2, adenosine, etc.); formula image Cardiomyocyte-Fibroblast signals (e.g. TGF-β, CTGF, etc.); formula image endocrine signals (e.g. adiponectin, adrenomedullin, intermedin, aldosterone etc.); formula image integrins; formula image connexins.
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