ArticleCell2019
Hypoxia Rescues Frataxin Loss by Restoring Iron Sulfur Cluster Biogenesis.
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Article in Cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.
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94citing papers in PubMed
10.0field-weighted citation impact, top 1% of its field
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Who cites it
94 citing papers in PubMed, 161 citations in OpenAlex.
- Significance of GSH and HRedox report : communications in free radical research · 2026Review
- A second-generation "hypoxia in a pill" rescues neurodegenerative phenotypes across distinct mouse models.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Article
- Autophagy dependent HIF1α proteostasis is compromised in models of PEX1 deficiencies.bioRxiv : the preprint server for biology · 2026Article
- Hypoxia rescues complex 1-associated disease caused by proteostatic defects.Nature metabolism · 2026Article
- Oxygen relief for a proteostasis-driven disease associated with mitochondrial complex I dysfunction.Nature metabolism · 2026Article
- Non-Mammalian Models for Mitochondria Research in CNS Disorders.Biomolecules · 2026Review
- Linoleic acid accelerates osteoarthritis progression in male rats by targeting iron-sulfur clusters to drive ferroptosis in chondrocytes.Nature communications · 2026Article
- Copper homeostasis and cuproptosis: molecular mechanisms and therapeutic opportunities.Molecular biomedicine · 2026Review
- The iron-sulfur cluster assembly factor FDX2 is required for tumor initiation but not for growth of established tumors in transplantation models.The Journal of biological chemistry · 2026Article
- Mitochondrial cardiomyopathy: bridging molecular mechanisms and clinical frontiers.Nature reviews. Cardiology · 2026Review
- Hydrogen sulfide increases intracellular oxygen and inhibits the HIF response.The Journal of biological chemistry · 2026Article
- Harnessing Cuproptosis resistance to advance cancer therapeutics.Apoptosis : an international journal on programmed cell death · 2026Review
- Article
- Ferroptosis is a novel pathogenic mechanism of FDXR-related disease via disruption of the NRF2 pathway.Cell death discovery · 2025Article
- Iron-deplete diet enhances Caenorhabditis elegans lifespan via oxidative stress response pathways.The EMBO journal · 2025Article
- A mouse model of MEPAN demonstrates a role for mitochondrial fatty acid synthesis in iron-sulfur cluster and supercomplex formation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Iron-deplete diet enhancesbioRxiv : the preprint server for biology · 2025Article
- Hypoxia ameliorates neurodegeneration and movement disorder in a mouse model of Parkinson's disease.Nature neuroscience · 2025Article
- XDH-1 inactivation causes xanthine stone formation in Caenorhabditis elegans which is inhibited by SULP-4-mediated anion exchange in the excretory cell.PLoS biology · 2025Article
34 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 5 institutions in 1 country.
Tslil AstBroad Institute, Cambridge, MA 02142, USA; Howard Hughes Medical Institute, Howard Hughes Medical Institute, Massachusetts General Hospital, Boston, MA 02114, USA; Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA; Harvard Medical School, Boston, MA 02115, USA.
Joshua D MeiselBroad Institute, Cambridge, MA 02142, USA; Howard Hughes Medical Institute, Howard Hughes Medical Institute, Massachusetts General Hospital, Boston, MA 02114, USA; Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA; Harvard Medical School, Boston, MA 02115, USA.
Shachin PatraDepartment of Chemistry, Texas A&M University, College Station, TX 77843, USA.
Hong WangBroad Institute, Cambridge, MA 02142, USA; Howard Hughes Medical Institute, Howard Hughes Medical Institute, Massachusetts General Hospital, Boston, MA 02114, USA; Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA; Harvard Medical School, Boston, MA 02115, USA.
Robert M H GrangeDepartment of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Boston, MA 02114, USA.
Sharon H KimBroad Institute, Cambridge, MA 02142, USA; Howard Hughes Medical Institute, Howard Hughes Medical Institute, Massachusetts General Hospital, Boston, MA 02114, USA; Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA; Harvard Medical School, Boston, MA 02115, USA.
Sarah E CalvoBroad Institute, Cambridge, MA 02142, USA; Howard Hughes Medical Institute, Howard Hughes Medical Institute, Massachusetts General Hospital, Boston, MA 02114, USA; Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA; Harvard Medical School, Boston, MA 02115, USA.
Lauren L OreficeDepartment of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA; Harvard Medical School, Boston, MA 02115, USA.
Fumiaki NagashimaDepartment of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Boston, MA 02114, USA.
Fumito IchinoseDepartment of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Boston, MA 02114, USA.
Warren M ZapolDepartment of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Boston, MA 02114, USA.
Gary RuvkunDepartment of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA; Harvard Medical School, Boston, MA 02115, USA.
David P BarondeauDepartment of Chemistry, Texas A&M University, College Station, TX 77843, USA.
Vamsi K MoothaBroad Institute, Cambridge, MA 02142, USA; Howard Hughes Medical Institute, Howard Hughes Medical Institute, Massachusetts General Hospital, Boston, MA 02114, USA; Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA; Harvard Medical School, Boston, MA 02115, USA. Electronic address: vamsi@hms.harvard.edu.
Massachusetts General Hospital · USHarvard University · USBroad Institute · USHoward Hughes Medical Institute · USTexas A&M University · US
Funding
GENETIC AND MOLECULAR BASIS OF LONGEVITYR01AG016636 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI GARY B RUVKUN · 1999 to 2026
$12.4MMitochondrial Parts, Pathways, and PathogenesisR35GM122455 · NIGMS · BROAD INSTITUTE, INC. · PI MOOTHA, VAMSI KRISHNA · 2017 to 2021
$4.0MStructure and Mechanism of the Human FE-S Cluster Assembly ComplexR01GM096100 · NIGMS · TEXAS A&M UNIVERSITY · PI BARONDEAU, DAVID P · 2011 to 2024
$3.5MHoward Hughes Medical InstituteNIA NIH HHS R01 AG016636NIGMS NIH HHS R01 GM096100NIGMS NIH HHS R35 GM122455
Abstract
Friedreich's ataxia (FRDA) is a devastating, multisystemic disorder caused by recessive mutations in the mitochondrial protein frataxin (FXN). FXN participates in the biosynthesis of Fe-S clusters and is considered to be essential for viability. Here we report that when grown in 1% ambient O
Indexed as
Activating Transcription Factor 4AnimalsCaenorhabditis elegansFemaleFrataxinFriedreich AtaxiaHEK293 CellsHumansHypoxiaIronIron-Binding ProteinsIron Regulatory Protein 2Iron-Sulfur ProteinsK562 CellsMaleMiceActivating Transcription Factor 4ATF4 protein, humanFrataxinIronIron-Binding ProteinsIron Regulatory Protein 2Iron-Sulfur ProteinsMitochondrial ProteinsNFE2L2 protein, humanNF-E2-Related Factor 2Sulfur
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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.