PGAM5 is a key driver of mitochondrial dysfunction in experimental lung fibrosis
Mitochondrial homeostasis has recently emerged as a focal point in the pathophysiology of idiopathic pulmonary fibrosis (IPF), but conflicting data have been reported regarding its regulation. We speculated that phosphoglycerate mutase family member 5 (PGAM5), a mitochondrial protein at the intersec...
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| Main Authors: | , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
5 June 2019
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| In: |
Cellular and molecular life sciences
Year: 2019, Volume: 76, Issue: 23, Pages: 4783-4794 |
| ISSN: | 1420-9071 |
| DOI: | 10.1007/s00018-019-03133-1 |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1007/s00018-019-03133-1
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| Author Notes: | Ingo Ganzleben, Gui-Wei He, Claudia Günther, Elena-Sophie Prigge, Karsten Richter, Ralf J. Rieker, Dimitrios Mougiakakos, Markus F. Neurath, Christoph Becker |
MARC
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| 520 | |a Mitochondrial homeostasis has recently emerged as a focal point in the pathophysiology of idiopathic pulmonary fibrosis (IPF), but conflicting data have been reported regarding its regulation. We speculated that phosphoglycerate mutase family member 5 (PGAM5), a mitochondrial protein at the intersection of multiple cell death and mitochondrial turnover pathways, might be involved in the pathogenesis of IPF. | ||
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