A Novel Role for Tumor Necrosis Factor–Like Weak Inducer of Apoptosis (TWEAK) in the Development of Cardiac Dysfunction and Failure
Author(s) -
Mohit Jain,
Aniela Jakubowski,
Lei Cui,
Jianru Shi,
Lihe Su,
Michael Bauer,
Jian Guan,
Chee Chew Lim,
Yoshiro Naito,
Jeffrey S. Thompson,
Flora Sam,
Christine Ambrose,
Michael Parr,
Thomas Crowell,
John Lincecum,
Monica Z. Wang,
YenMing Hsu,
Timothy S. Zheng,
Jennifer S. Michaelson,
Ronglih Liao,
Linda C. Burkly
Publication year - 2009
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.108.837286
Subject(s) - medicine , tumor necrosis factor alpha , cancer research , cardiomyopathy , cytokine , heart failure , pathogenesis , fibrosis , dilated cardiomyopathy , apoptosis , receptor , downregulation and upregulation , immunology , biology , gene , genetics
Tumor necrosis factor-like weak inducer of apoptosis (TWEAK), a member of the tumor necrosis factor superfamily, is a multifunctional cytokine known to regulate cellular functions in contexts of injury and disease through its receptor, fibroblast growth factor-inducible molecule 14 (Fn14). Although many of the processes and downstream signals regulated by the TWEAK/Fn14 pathway have been implicated in the development of cardiac dysfunction, the role of TWEAK in the cardiovascular system is completely unknown.
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