PGAM5 is a key driver of mitochondrial dysfunction in experimental lung fibrosis

Rationale 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 th...

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Veröffentlicht in:	Cellular and molecular life sciences : CMLS 2019-12, Vol.76 (23), p.4783-4794
Hauptverfasser:	Ganzleben, Ingo, He, Gui-Wei, Günther, Claudia, Prigge, Elena-Sophie, Richter, Karsten, Rieker, Ralf J., Mougiakakos, Dimitrios, Neurath, Markus F., Becker, Christoph
Format:	Artikel
Sprache:	eng
Schlagworte:	A549 Cells Animals Biochemistry Biomedical and Life Sciences Biomedicine Bleomycin Bleomycin - pharmacology Cell Biology Cell death Damage Depolarization Disease Models, Animal Epithelial cells Fibrosis Flow cytometry Gene Editing Homeostasis Humans Life Sciences Lung diseases Membrane potential Membrane Potential, Mitochondrial - drug effects Mice Mice, Knockout Microtubule-Associated Proteins - metabolism Mitochondria Mitochondria - drug effects Mitochondria - metabolism Mitophagy - drug effects Original Original Article Pathogenesis Phosphoglycerate mutase Phosphoprotein Phosphatases - genetics Phosphoprotein Phosphatases - metabolism Protein Kinases - metabolism Pulmonary fibrosis Pulmonary Fibrosis - metabolism Pulmonary Fibrosis - pathology Reactive Oxygen Species - metabolism Structure-function relationships Target recognition Therapeutic applications Transmission electron microscopy
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