Local Tenomodulin Absence, Angiogenesis, and Matrix Metalloproteinase Activation Are Associated With the Rupture of the Chordae Tendineae Cordis
Author(s) -
Naritaka Kimura,
Chisa Shukunami,
Daihiko Hakuno,
Masatoyo Yoshioka,
Shigenori Miura,
Denitsa Docheva,
Takehiro Kimura,
Yasunori Okada,
Goki Matsumura,
Toshiharu Shinoka,
Ryohei Yozu,
Junjiro Kobayashi,
Hatsue IshibashiUeda,
Yuji Hiraki,
Keiichi Fukuda
Publication year - 2008
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.108.780031
Subject(s) - medicine , angiogenesis , matrix metalloproteinase , vascular endothelial growth factor , pathology , anatomy , vegf receptors
Rupture of the chordae tendineae cordis (CTC) is a well-known cause of mitral regurgitation. Despite its importance, the mechanisms by which the CTC is protected and the cause of its rupture remain unknown. CTC is an avascular tissue. We investigated the molecular mechanisms underlying the avascularity of CTC and the correlation between avascularity and CTC rupture.
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