ArticleFrontiers in bioscience (Landmark edition)2022
AMPK Signaling Regulates Mitophagy and Mitochondrial ATP Production in Human Trophoblast Cell Line BeWo.
Article in Frontiers in bioscience (Landmark edition), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- MUC1 Protects Preimplantation Embryos In Vitro via Clearance of ROS by Triggering Mitophagy.Cells · 2026Article
- Mitophagy: A key regulator in the pathophysiology and treatment of spinal cord injury.Neural regeneration research · 2026Article
- RNA-seq analysis of mitochondria-related genes regulated by AMPK in the human trophoblast cell line BeWo.Animal models and experimental medicine · 2025Article
- Administration of AICAR, an AMPK Activator, Prevents and Reverses Diabetic Polyneuropathy (DPN) by Regulating Mitophagy.International journal of molecular sciences · 2024Article
- Poricoic acid a ameliorates high glucose-induced podocyte injury by regulating the AMPKα/FUNDC1 pathway.Molecular biology reports · 2024Article
- 2-Bromopalmitate depletes lipid droplets to inhibit viral replication.Journal of virology · 2024Article
- Biomarkers for Diagnosing and Treating Fetal Growth Restriction.Current medicinal chemistry · 2024Review
- Natural Drugs: A New Direction for the Prevention and Treatment of Diabetes.Molecules (Basel, Switzerland) · 2023Review
- The Role of Autophagy in the Female Reproduction System: For Beginners to Experts in This Field.Biology · 2023Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
introductionAccumulating evidence suggests that mitochondrial structural and functional defects are present in human placentas affected by pregnancy related disorders, but mitophagy pathways in human trophoblast cells/placental tissues have not been investigated.
methodsIn this study, we investigated three major mitophagy pathways mediated by PRKN, FUNDC1, and BNIP3/BNIP3L in response to AMPK activation by AICAR and knockdown of
resultsAutophagy flux assay demonstrated that AMPK signaling activation stimulates autophagy, evidenced increased LC3II and SQSTM1 protein abundance in the whole cell lysates and mitochondrial fractions, and mitophagy flux assay demonstrated that the activation of AMPK signaling stimulates mitophagy via PRKN and FUNDC1 mediated but not BNIP3/BNIP3L mediated pathways. The stimulatory regulation of AMPK signaling on mitophagy was confirmed by AKD which reduced the abundance of LC3II, SQSTM1, PRKN, and FUNDC1 proteins, but increased the abundance of BNIP3/BNIP3L proteins. Coincidently, AKD resulted in elevated mitochondrial membrane potential and reduced mitochondrial ATP production, compared to control BeWo cells.
conclusionsIn summary, AMPK signaling stimulates mitophagy in human trophoblast cells via PRKN and FUNDC1 mediated mitophagy pathways and AMPK regulated mitophagy contributes to the maintenance of mitochondrial membrane potential and mitochondrial ATP production.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.