| Autor: |
Rasanen, Markus O, Jennifer, Paech, Hemanthakumar, Karthik Amudhala, Sultan, Ibrahim, Yu, Wei, He, Liqun, Tang, Juan, Sun, Ying, Hlushchuk, Ruslan, Khoma, Oleksiy-Zakhar, Mervaala, Eero M, Djonov, Valentin, Betsholtz, Christer, Kivel?, Riikka, Zhou, Bin, Alitalo, Kari K |
| Zdroj: |
Circulation (Ovid); November 2019, Vol. 140 Issue: Supplement 1 pA16509-A16509, 1p |
| Abstrakt: |
In coronary artery disease, especially in hypertensive patients, the subendocardial myocardium is vulnerable to ischemia and myocardial infarction (MI), because it is the most distant target of coronary perfusion. Currently, coronary occlusion is treated mainly by catheter-assisted reperfusion and thrombolysis of the coronary vessels. However, regardless of the reperfusion, insufficient subendocardial vessel perfusion (?no-flow reperfusion?) occurs frequently. Recent discoveries have indicated that in the developing heart, sinus venosus and endocardium are the major sources of coronary vessels that support the expanding myocardium, but the adult endocardium can no longer generate new blood vessels because the endocardium-to-coronary vessel transition is inhibited after the neonatal stage. Herewe show that cardiomyocyte overexpression of VEGF-B in mice and rats promotes growth of vessels derived from the endocardium that perfuse of the subendocardial myocardium. Subendocardial endothelial cell activation and proliferation was obtained in adult mice by VEGF-B produced by gene delivery to the cardiomyocytes. Importantly, VEGF-B promoted endocardial to vascular endothelial cell reprogramming and endocardium-derived vessel invasion into the myocardium during tissue remodeling after MI. Thus, re-activation and reprogramming of adult endocardium by growth factors could be a new therapeutic strategy for cardiac neovascularization after myocardial ischemic injury. |
| Databáze: |
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