Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/41565
Title: Impaired mitochondrial fusion, autophagy, biogenesis and dysregulated lipid metabolism is associated with preeclampsia.
Authors: Zhou, X.
Han, T-L.
Chen, H.
Baker, Philip N.
Qi, H.
Zhang, H.
First Published: 25-Jul-2017
Publisher: Elsevier
Citation: Experimental Cell Research, 2017, 359 (1), pp. 195-204
Abstract: Preeclampsia(PE) is a pregnancy complication that is diagnosed by the new onset of hypertension and proteinuria. The etiology of PE remains unclear; however, growing evidence indicates that mitochondrial impairment contributes to the pathogenesis. Therefore, we aim to investigate the function of mitochondria in the development of PE. The mitochondrial metabolome in preeclamptic (n = 11) and normal (n = 11) placentas were analyzed using Gas chromatography-mass spectrometry (GC-MS). Student's t-tests and receiver operating characteristic (ROC) curves were conducted to determine which mitochondrial metabolites differed significantly between the two groups. The Pathway Activity Profiling (PAPi) R package was used to predict which metabolic pathways were affected by PE. Western blot analysis was performed to identify the candidate proteins which were associated with mitochondrial repair regulation. GC-MS analysis demonstrated that higher levels of 38 metabolites and lower levels of 2 metabolites were observed in the placenta of patients with severe PE (sPE). Five fatty acids had an area under the ROC curve above 90%. Furthermore, we revealed abnormal regulation of mitochondrial dynamics, autophagy, and biogenesis in sPE. Our discoveries indicate that the compromised lipid metabolism in sPE may result from dysfunctional mitochondria, thus revealing new insights into the etiology of the disease.
DOI Link: 10.1016/j.yexcr.2017.07.029
ISSN: 0014-4827
eISSN: 1090-2422
Links: https://www.sciencedirect.com/science/article/pii/S0014482717304019?via%3Dihub
http://hdl.handle.net/2381/41565
Embargo on file until: 25-Jul-2018
Version: Post-print
Status: Peer-reviewed
Type: Journal Article
Rights: Copyright © 2017, Elsevier. Deposited with reference to the publisher’s open access archiving policy. (http://www.rioxx.net/licenses/all-rights-reserved)
Description: The file associated with this record is under embargo until 12 months after publication, in accordance with the publisher's self-archiving policy. The full text may be available through the publisher links provided above.
Appears in Collections:Published Articles, College of Medicine, Biological Sciences and Psychology

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