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  Defective mitochondrial cardiolipin remodeling dampens HIF-1 alpha expression in hypoxia.

Chowdhury, A., Aich, A., Jain, G., Wozny, K., Lüchtenborg, C., Hartmann, M., et al. (2018). Defective mitochondrial cardiolipin remodeling dampens HIF-1 alpha expression in hypoxia. Cell Reports, 25(3), 561-570. doi:10.1016/j.celrep.2018.09.057.

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Item Permalink: http://hdl.handle.net/21.11116/0000-0002-6EF9-B Version Permalink: http://hdl.handle.net/21.11116/0000-0002-6F00-2
Genre: Journal Article

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 Creators:
Chowdhury, A., Author
Aich, A., Author
Jain, G., Author
Wozny, K., Author
Lüchtenborg, C., Author
Hartmann, M., Author
Bernhard, O., Author
Balleiniger, M., Author
Alfar, E. A., Author
Zieseniss, A., Author
Toischer, K., Author
Guan, K. M., Author
Rizzoli, S. O., Author
Brügger, B., Author
Fischer, A., Author
Katschinski, D. M., Author
Rehling, P.1, Author              
Dudek, J., Author
Affiliations:
1Max Planck Fellow Peter Rehling, ou_1298545              

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 Abstract: Mitochondria fulfill vital metabolic functions and act as crucial cellular signaling hubs, integrating their metabolic status into the cellular context. Here, we show that defective cardiolipin remodeling, upon loss of the cardiolipin acyl transferase tafazzin, decreases HIF-1 alpha signaling in hypoxia. Tafazzin deficiency does not affect posttranslational HIF-1 alpha regulation but rather HIF-1 alpha gene expression, a dysfunction recapitulated in iPSC-derived cardiomyocytes from Barth syndrome patients with tafazzin deficiency. RNA-seq analyses confirmed drastically altered signaling in tafazzin mutant cells. In hypoxia, tafazzin-deficient cells display reduced production of reactive oxygen species (ROS) perturbing NF-kappa B activation and concomitantly HIF-1 alpha gene expression. Tafazzin-deficient mice hearts display reduced HIF-1 alpha levels and undergo maladaptive hypertrophy with heart failure in response to pressure overload challenge. We conclude that defective mitochondria! cardiolipin remodeling dampens HIF-1 alpha signaling due to a lack of NF-kappa B activation through reduced mitochondrial ROS production, decreasing HIF-1 alpha transcription.

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Language(s): eng - English
 Dates: 2018-10-16
 Publication Status: Published online
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Method: Peer
 Identifiers: DOI: 10.1016/j.celrep.2018.09.057
 Degree: -

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Title: Cell Reports
Source Genre: Journal
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Pages: - Volume / Issue: 25 (3) Sequence Number: - Start / End Page: 561 - 570 Identifier: -