2019
DOI: 10.1016/j.cell.2018.12.023
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Abstract: Highlights d Artery endothelial cells (ECs) of neonatal hearts have a unique response to injury d Injury stimulates artery cell migration and reassembly into collateral arteries d CXCL12-CXCR4 signaling guides artery reassembly, facilitating heart regeneration d Adult artery ECs can be induced to undergo artery reassembly with exogenous CXCL12

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Cited by 168 publications
(220 citation statements)
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“…caErbb2 was induced for 3 weeks, representing ~ 2.5 weeks of ERBB2 expression, and was consistently characterized by ventricular wall hypertrophy and lumen shrinkage, which resulted in a transient increase in ejection fraction (Figure1B-D To begin investigating the underlying cellular characteristics of OE CMs, we performed bulk RNA -seq comparing injured WT and OE hearts. We analyzed enriched hallmark gene sets using GSEA, which highlighted epithelial to mesenchymal transition (EMT) with the highest enrichment score ( Figure 1H, Figure S2A) among other hallmarks previously implicated in cardiac regeneration, such as hypoxia (Kimura et al, 2015) (Nakada et al, 2016), angiogenesis (Marín-juez et al, 2016) (Das et al, 2019) and glycolysis (Honkoop et al, 2019) (Fukuda et al, 2019). Although the myocardium is not an epithelial tissue, EMT-like behaviors such as ECM-deposition and degradation, and CM migration are in line with the requirements for tissue replacement and regeneration in the context of a pre-existing scar.…”
Section: Delayed Erbb2 Induction In An Hf Model Triggers Functional Rmentioning
confidence: 99%
“…caErbb2 was induced for 3 weeks, representing ~ 2.5 weeks of ERBB2 expression, and was consistently characterized by ventricular wall hypertrophy and lumen shrinkage, which resulted in a transient increase in ejection fraction (Figure1B-D To begin investigating the underlying cellular characteristics of OE CMs, we performed bulk RNA -seq comparing injured WT and OE hearts. We analyzed enriched hallmark gene sets using GSEA, which highlighted epithelial to mesenchymal transition (EMT) with the highest enrichment score ( Figure 1H, Figure S2A) among other hallmarks previously implicated in cardiac regeneration, such as hypoxia (Kimura et al, 2015) (Nakada et al, 2016), angiogenesis (Marín-juez et al, 2016) (Das et al, 2019) and glycolysis (Honkoop et al, 2019) (Fukuda et al, 2019). Although the myocardium is not an epithelial tissue, EMT-like behaviors such as ECM-deposition and degradation, and CM migration are in line with the requirements for tissue replacement and regeneration in the context of a pre-existing scar.…”
Section: Delayed Erbb2 Induction In An Hf Model Triggers Functional Rmentioning
confidence: 99%
“…After MI, the expression of ZEB1 is significantly induced in mice . ZEB1 has been reported to bind at the promoter of CXCR4 gene, which seems to restore cardiac fibrosis, to inhibit the expression of CXCR4 in human cardiac cells to aggravate MI . Moreover, overexpression of ZEB1 up‐regulates the expressions of collagen crosslinking enzymes as well as the expressions of Col1A1 and Col3A1 to mediate collagen stabilization and deposition of ECM .…”
Section: Introductionmentioning
confidence: 99%
“…In zebrafish, delayed angiogenesis within the infarct zone reduces cardiomyocyte proliferation and results in nonresolution of scar [22] [64]. Additionally, in Hippo-deficient cardiomyocytes, upregulation of vasculogenesis [65] stimulates development of collateral vessel networks that are essential for tissue regeneration [66]. Furthermore, exogenous application of CXCL12 (chemotactic ligand induced by hypoxia) on the epicardium induces formation of collateral vessels by migration of arterial endothelial cells along pre-existing capillaries (arterial re-assembly) [66] [67].…”
Section: Physiopathology Of Cell Death and Myocardial Remodelingmentioning
confidence: 99%
“…Additionally, in Hippo-deficient cardiomyocytes, upregulation of vasculogenesis [65] stimulates development of collateral vessel networks that are essential for tissue regeneration [66]. Furthermore, exogenous application of CXCL12 (chemotactic ligand induced by hypoxia) on the epicardium induces formation of collateral vessels by migration of arterial endothelial cells along pre-existing capillaries (arterial re-assembly) [66] [67]. An additional element of cardiac repair that is the formation of lymph vessels within the ischemic region; stimulation of lymphangiogenesis after infarction is necessary for removal of inflammatory cells and cellular by-products from the zone under repair [68].…”
Section: Physiopathology Of Cell Death and Myocardial Remodelingmentioning
confidence: 99%