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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Nat+Commun
2017 ; 8
(1
): 578
Nephropedia Template TP
Wang Y
; Wu B
; Lu P
; Zhang D
; Wu B
; Varshney S
; Del Monte-Nieto G
; Zhuang Z
; Charafeddine R
; Kramer AH
; Sibinga NE
; Frangogiannis NG
; Kitsis RN
; Adams RH
; Alitalo K
; Sharp DJ
; Harvey RP
; Stanley P
; Zhou B
Nat Commun
2017[Sep]; 8
(1
): 578
PMID28924218
show ga
Coronary artery anomalies may cause life-threatening cardiac complications;
however, developmental mechanisms underpinning coronary artery formation remain
ill-defined. Here we identify an angiogenic cell population for coronary artery
formation in mice. Regulated by a DLL4/NOTCH1/VEGFA/VEGFR2 signaling axis, these
angiogenic cells generate mature coronary arteries. The NOTCH modulator POFUT1
critically regulates this signaling axis. POFUT1 inactivation disrupts signaling
events and results in excessive angiogenic cell proliferation and plexus
formation, leading to anomalous coronary arteries, myocardial infarction and
heart failure. Simultaneous VEGFR2 inactivation fully rescues these defects.
These findings show that dysregulated angiogenic precursors link coronary
anomalies to ischemic heart disease.Though coronary arteries are crucial for
heart function, the mechanisms guiding their formation are largely unknown. Here,
Wang et al. identify a unique, endocardially-derived angiogenic precursor cell
population for coronary artery formation in mice and show that a
DLL4/NOTCH1/VEGFA/VEGFR2 signaling axis is key for coronary artery development.