ArticleCell death & disease2018
Iron overload promotes mitochondrial fragmentation in mesenchymal stromal cells from myelodysplastic syndrome patients through activation of the AMPK/MFF/Drp1 pathway.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 110 citations in OpenAlex.
- Spatial AuAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Forged in iron: molecular insights into iron tolerance in Hermetia illucens.NPJ science of food · 2026Article
- Therapeutic Potential of Deferiprone-Resveratrol Hybrid (DFP-RVT) Against Hepatic Iron Overload in β-Thalassemia Mice: A Proteomic Analysis.Biomolecules · 2026Article
- Cellular iron flux measurement by micromagnetic resonance relaxometry as a critical quality attribute of mesenchymal stromal cells.Stem cells translational medicine · 2026Article
- The Role of Iron-Overloaded Macrophages in Mesenchymal Stem Cell Senescence and Anemia in Myelodysplastic Syndromes: Protocol for an In Vitro Study.JMIR research protocols · 2026Article
- Crosstalk Between Microbiome and Ferroptosis in Diseases: From Mechanism to Therapy.Comprehensive Physiology · 2025Review
- Ferritin in Acute Myeloid Leukemia: Not Only a Marker of Inflammation and Iron Overload, but Also a Regulator of Cellular Iron Metabolism, Signaling and Communication.International journal of molecular sciences · 2025Review
- The role of mitochondria in iron overload-induced damage.Journal of translational medicine · 2024Review
- The hepcidin-ferroportin axis influences mitochondrial function, proliferation, and migration in pulmonary artery endothelial and smooth muscle cells.Pulmonary circulation · 2024Article
- Drp1 depletion protects against ferroptotic cell death by preserving mitochondrial integrity and redox homeostasis.Cell death & disease · 2024Article
- Pretreatment can alleviate programmed cell death in mesenchymal stem cells.World journal of stem cells · 2024Article
- RSL3 enhances ROS-mediated cell apoptosis of myelodysplastic syndrome cells through MYB/Bcl-2 signaling pathway.Cell death & disease · 2024Article
- Iron regulates the quiescence of naive CD4 T cells by controlling mitochondria and cellular metabolism.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Role of reactive oxygen species in myelodysplastic syndromes.Cellular & molecular biology letters · 2024Review
- Potential application of traditional Chinese medicine in age-related macular degeneration-focusing on mitophagy.Frontiers in pharmacology · 2024Review
- The impact of granulocyte colony-stimulating factor and decitabine-containing conditioning in myelodysplastic syndrome patients with iron overload undergoing allogeneic hematopoietic stem cell transplantation: a retrospective study.Therapeutic advances in hematology · 2024Article
- Exenatide-Modified Deferoxamine-Based Nanoparticles Ameliorates Neurological Deficits in Parkinson's Disease Mice.International journal of nanomedicine · 2024Article
- The circSNX14 functions as a tumor suppressor via the miR-562/ LATS2 pathway in hepatocellular carcinoma cells.Journal of molecular histology · 2023Article
- The polyHIS Tract of Yeast AMPK Coordinates Carbon Metabolism with Iron Availability.International journal of molecular sciences · 2023Article
- AMPK/MFF Activation: Role in Mitochondrial Fission and Mitophagy in Dry Eye.Investigative ophthalmology & visual science · 2022Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Iron overload (IO) has been reported to contribute to mesenchymal stromal cell (MSC) damage, but the precise mechanism has yet to be clearly elucidated. In this study, we found that IO increased cell apoptosis and lowered cell viability in MSCs, accompanied by extensive mitochondrial fragmentation and autophagy enhancement. All these effects were reactive oxygen species (ROS) dependent. In MSCs with IO, the ATP concentrations were significantly reduced due to high ROS levels and low electron respiratory chain complex (ETC) II/III activity. Reduced ATP phosphorylated AMP-activated protein kinase (AMPK). Activation of AMPK kinase complexes triggered mitochondrial fission. Moreover, gene knockout of AMPK via CRISPR/Cas9 reduced cell apoptosis, enhanced cell viability and attenuated mitochondrial fragmentation and autophagy caused by IO in MSCs. Further, AMPK-induced mitochondrial fragmentation of MSCs with IO was mediated via phosphorylation of mitochondrial fission factor (MFF), a mitochondrial outer-membrane receptor for the GTPase dynamin-related protein 1 (Drp1). Gene knockdown of MFF reversed AMPK-induced mitochondrial fragmentation in MSCs with IO. In addition, MSCs from IO patients with myelodysplastic syndrome (MDS) showed increased cell apoptosis, decreased cell viability, higher ROS levels, lower ATP concentrations and increased mitochondrial fragmentation compared with MSCs from non-IO patients. In addition, iron chelation or antioxidant weakened the activity of the AMPK/MFF/Drp1 pathway in MDS-MSCs with IO from several patients, accompanied by attenuation of mitochondrial fragmentation and autophagy. Taken together, the AMPK/MFF/Drp1 pathway has an important role in the damage to MDS-MSCs caused by IO.
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