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Review
. 2009 Dec 15;120(24):2496-508.
doi: 10.1161/CIRCULATIONAHA.107.751412.

Electrophysiological challenges of cell-based myocardial repair

Huei-Sheng Vincent Chen  1 , Changsung Kim, Mark Mercola
Affiliations
Review

Electrophysiological challenges of cell-based myocardial repair

Huei-Sheng Vincent Chen et al. Circulation. .
No abstract available

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Figures

Figure 1
Figure 1
A simple schematic of molecular pathways of cardiogenesis. See reviews in 9–13 for details. Shaded areas indicate the extra-cardiac cell sources. Dkk1 indicates Dickkopf1; Sox17, an endodermal transcription factor; TCF, T cell factor; BMP, Bone morphogenetic protein; Wnts, Wingless related factors; Nkx, NK family of Homeobox genes; MEF2C, myocyte-specific enhancer-binding factor 2C; Tbx, T-box transcription factors; Flk1, kinase insert domain protein receptor; Isl1: LIM homeodomain transcription factor islet1; FGF, Fibroblast growth factor; EphB, Ephrin-B; PitX, Pituitary homeobox family; NRG-1, neuregulin-1; RA, retinoid acid; ET1, endothelin-1; Hrt, hairy-related transcription factor; BOP, CD8b-opposite transcription factor; Foxh1, forkhead DNA binding transcription factor; Fox, forkhead transcription factor; and * denotes mesenchymal cells from multiple sources.
Figure 2
Figure 2
A diagram of genetic and signaling pathways involved in chamber specification of myocardial development. JAG indicates a notch ligand, Jagged; Irx, Iroquois-related homeobox protein; see Figure 1 legend for the definition of other abbreviations. Adapted from reference with permission.
Figure 3
Figure 3
Expression patterns of connexin 43 (Cx43) in human embryonic stem cell-derived cardiomyocytes (hESC-CMs) and neonatal rat ventricular myocytes (NRVMs). Images are of hESC-CMs in cardiospheres (A–C) and in co-cultures with NRVMs (D–F). hESC-CMs were stained with anti-Cx43 (green) (A), anti-N-cadherin (red) (B), anti-α-actinin (blue), and anti-human nuclear antigen (hNA, blue) (merged in C). In the co-culture of hESC-CMs and NRVMs, myocytes were immunostained with anti-Cx43 (green) (D), anti-hNA and cardiac troponin I (cTnI) (both in red, E), as well as DAPI for nuclear staining (blue) (merged in F). In E, F, only human cells are positive for anti-hNA staining (red). hESC-CMs are variable in size. Cxs 43 of both hESC-CMs and NRVMs distribute in a punctate and neonatal-like pattern at the cell contact surfaces.
Figure 4
Figure 4
Summary of potential arrhythmogenic mechanisms of cell-based therapies.
See this image and copyright information in PMC

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