ArticleCell death & disease2022
Oxidative degradation of dihydrofolate reductase increases CD38-mediated ferroptosis susceptibility.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 20 citations in OpenAlex.
- Individualized treatment and key prognostic biomarkers based on folate metabolism in patients with pancreatic cancer.Translational cancer research · 2026Article
- Expression of CD38Scientific reports · 2026Article
- Nicotinamide mononucleotide alleviates the streptozotocin-mediated ferroptosis of islet β-cells via the Nrf2/GPX4 pathway.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas · 2026Article
- Disruption of Gut Microbiota-Mediated De Novo NADAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- NADK Governs Ferroptosis Susceptibility by Orchestrating NADPH Homeostasis.Antioxidants (Basel, Switzerland) · 2025Article
- Mechanisms of ferroptosis in primary hepatocellular carcinoma and progress of artificial intelligence-based predictive modeling in hepatocellular carcinoma.World journal of gastroenterology · 2025Review
- The inducible role of autophagy in cell death: emerging evidence and future perspectives.Cell communication and signaling : CCS · 2025Review
- Mechanism of Ferroptosis and Its Role in Disease Development.International journal of biological sciences · 2025Review
- The molecular and metabolic landscape of ferroptosis in respiratory diseases: Pharmacological aspects.Journal of pharmaceutical analysis · 2025Review
- Nicotinamide mononucleotide protects STAT1 from oxidative stress-induced degradation to prevent colorectal tumorigenesis.MedComm · 2024Article
- Emerging roles of ferroptosis in pulmonary fibrosis: current perspectives, opportunities and challenges.Cell death discovery · 2024Review
- International consensus guidelines for the definition, detection, and interpretation of autophagy-dependent ferroptosis.Autophagy · 2024Review
- Supplementing Boar Diet with Nicotinamide Mononucleotide Improves Sperm Quality Probably through the Activation of the SIRT3 Signaling Pathway.Antioxidants (Basel, Switzerland) · 2024Article
- Top Five Stories of the Cellular Landscape and Therapies of Atherosclerosis: Current Knowledge and Future Perspectives.Current medical science · 2024Review
- SIRT1 activated by AROS sensitizes glioma cells to ferroptosis via induction of NAD+ depletion-dependent activation of ATF3.Redox biology · 2024Article
- NADTheranostics · 2024Article
- Photodynamic Therapy Combined with Ferroptosis Is a Synergistic Antitumor Therapy Strategy.Cancers · 2023Review
- Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High expression of CD38 in tissues is a characteristic of aging, resulting in a decline in nicotinamide adenine dinucleotide (NAD) and increasing cellular reactive oxygen species (ROS). However, whether CD38 increases susceptibility to ferroptosis remains largely unexplored. Our previous study showed that CD38 overexpression decreased dihydrofolate reductase (DHFR). In the present study, we confirmed that high expression of CD38 increased ROS levels and induced DHFR degradation, which was prevented by nicotinamide mononucleotide (NMN) replenishment. We further revealed that ROS-mediated sulfonation on Cys7 of DHFR induced its degradation via the autophagy and non-canonical proteasome pathways. Mutation of Cys7 to alanine abolished ROS-induced DHFR degradation. Moreover, oxidative degradation of DHFR was responsible for the increased ferroptosis susceptibility of cells in which CD38 was highly expressed. We also found that CD38 expression was higher in bone-marrow-derived macrophages (BMDMs) from aged mice than those from young mice, while the DHFR level was lower. Consequently, we demonstrated that BMDMs from aged mice were more susceptible to ferroptosis that can be reverted by NMN replenishment, suggesting that CD38 high expression rendered cells more susceptible to ferroptosis. Taken together, these results indicated that CD38-mediated NAD
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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.