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Official PDF TranslationActa Biochimica et Biophysica Sinica

Excessive ER-phagy mediated by FAM134B contributes to trophoblast cell mitochondrial dysfunction in preeclampsia

Authors: Andi Wang; Zhuo Li; Dan Zhang; Chang Chen; Hua Zhang

DOI: 10.3724/abbs.2024065Status: Verified Translated Edition
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Key Findings in This Report

• FAM134B-mediated excessive ER-phagy is linked to trophoblast mitochondrial dysfunction in preeclampsia. • Increased FAM134B, IP3R, calnexin, cleaved caspase 3, and cytochrome C are observed in PE placentas and SNP-treated trophoblast cells. • Overexpression of FAM134B impairs trophoblast invasion and mitochondrial function, while autophagy inhibition rescues mitochondrial performance. • Excessive ER-phagy is associated with elevated gamma linolenic acid, suggesting a lipidomic link in PE pathogenesis.