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Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Proc+Natl+Acad+Sci+U+S+A 2015 ; 112 (52): E7276-85 Nephropedia Template TP
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Antifungal drug itraconazole targets VDAC1 to modulate the AMPK/mTOR signaling axis in endothelial cells #MMPMID26655341
Head SA; Shi W; Zhao L; Gorshkov K; Pasunooti K; Chen Y; Deng Z; Li Rj; Shim JS; Tan W; Hartung T; Zhang J; Zhao Y; Colombini M; Liu JO
Proc Natl Acad Sci U S A 2015[Dec]; 112 (52): E7276-85 PMID26655341show ga
Tumors promote angiogenesis to facilitate their growth and metastasis; thus, inhibition of angiogenesis is a promising strategy for treating cancer. During angiogenesis, endothelial cells (EC) are stimulated by proangiogenic factors to proliferate and migrate, leading to the formation of new blood vessels. Understanding the mechanisms regulating EC function therefore is essential for the development of new antiangiogenic interventions. Here, we identify a novel mechanism of EC regulation by the recently discovered angiogenesis inhibitor itraconazole, mediated by direct binding to the mitochondrial protein voltage-dependent anion channel 1 (VDAC1). VDAC1 inhibition perturbs mitochondrial ATP production, leading to activation of the AMP-activated protein kinase pathway and subsequent inhibition of mechanistic target of rapamycin, a regulator of EC proliferation. This study suggests VDAC1 may serve as a new therapeutic target for angiogenesis inhibition.