ArticleNature metabolism2020
MESH1 is a cytosolic NADPH phosphatase that regulates ferroptosis.
Article in Nature metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers.
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119 citing papers in PubMed, 171 citations in OpenAlex.
- Targeting ferroptosis in cancer: molecular mechanisms and emerging therapeutic strategies.Biochemistry and biophysics reports · 2026Review
- Ferroptosis in cancer: molecular mechanisms, tumour microenvironment, therapeutic resistance, and clinical translation.Journal of the Egyptian National Cancer Institute · 2026Review
- Pharmacological targeting of ferroptosis in cancer: mechanisms, tumor immunity, and translational challenges.Pharmacological reports : PR · 2026Review
- MESH1 regulates sulfation through the hydrolysis of PAPS.Nature chemical biology · 2026Article
- MESH1 functions as a metazoan PAPS phosphatase to regulate sulfation.Nature chemical biology · 2026Article
- Integrated analyses of in vivo mouse models and liver organoids reveal MFG-E8-mediated protection against hepatocyte injury.American journal of physiology. Gastrointestinal and liver physiology · 2026Article
- From the Cosmos to the Cell: The Central Role of Iron in the Chemistry and Evolution of Life.International journal of molecular sciences · 2026Review
- Immunometabolic reprogramming of macrophages by miR-423-5p-enriched small extracellular vesicles delivered via glucose/ROS-responsive hydrogel for diabetic wound healing.Journal of nanobiotechnology · 2026Article
- MESH1-mediated coenzyme A degradation drives ferroptosis sensitivity and muscle pathology.The Journal of clinical investigation · 2026Article
- Target sequence-conditioned design of peptide binders using masked language modeling.Nature biotechnology · 2026Article
- Ferroptosis-driven metabolic reprogramming in macrophages: Reshaping glucose utilization landscapes.Chinese medical journal · 2026Review
- Targeting ferroptosis in cancer: from mechanistic insights to therapeutic approaches.Molecular biomedicine · 2026Review
- Identification of 4,5,6,7-Tetrabromo-1bioRxiv : the preprint server for biology · 2026Article
- Characterization of the enzymatic activity of the rhythmic human NADP(H) phosphatase, Nocturnin.Archives of biochemistry and biophysics · 2026Article
- Regulation of apoptosis, ferroptosis, and pyroptosis mediated by acetylation.Cell death discovery · 2026Review
- Ferroptosis in diabetic retinopathy: from pathogenic mechanisms to translational prospects.Frontiers in endocrinology · 2026Review
- Disulfidptosis: A Metabolic Cell Death Mechanism with Therapeutic Potential in Cancer.Oncology research · 2026Review
- Research progress on the mechanism of tumor cell ferroptosis regulation by epigenetics.Epigenetics · 2025Review
- Keeping up with the nicotinamides: NADP(H), the forgotten circadian cofactor that keeps metabolic time.Life metabolism · 2025Review
- NADK Governs Ferroptosis Susceptibility by Orchestrating NADPH Homeostasis.Antioxidants (Basel, Switzerland) · 2025Article
59 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
Abstract
Critical to the bacterial stringent response is the rapid relocation of resources from proliferation toward stress survival through the respective accumulation and degradation of (p)ppGpp by RelA and SpoT homologues. While mammalian genomes encode MESH1, a homologue of the bacterial (p)ppGpp hydrolase SpoT, neither (p)ppGpp nor its synthetase has been identified in mammalian cells. Here, we show that human MESH1 is an efficient cytosolic NADPH phosphatase that facilitates ferroptosis. Visualization of the MESH1-NADPH crystal structure revealed a bona fide affinity for the NADPH substrate. Ferroptosis-inducing erastin or cystine deprivation elevates MESH1, whose overexpression depletes NADPH and sensitizes cells to ferroptosis, whereas MESH1 depletion promotes ferroptosis survival by sustaining the levels of NADPH and GSH and by reducing lipid peroxidation. The ferroptotic protection by MESH1 depletion is ablated by suppression of the cytosolic NAD(H) kinase, NADK, but not its mitochondrial counterpart NADK2. Collectively, these data shed light on the importance of cytosolic NADPH levels and their regulation under ferroptosis-inducing conditions in mammalian cells.
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