ArticleCell reports2022
Inhibition of glutaminolysis restores mitochondrial function in senescent stem cells.
Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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The trial behind it
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Who cites it
28 citing papers in PubMed, 35 citations in OpenAlex.
- Inhibiting Glutaminase Reverses Senescence-Associated Mitochondrial Dysfunction and Skeletal Muscle Decline.Aging cell · 2026Article
- Review
- Review
- Glutamate accumulation in myelofibrosis microenvironment rewires mesenchymal stromal cells metabolic and epigenetic profiles.Cell communication and signaling : CCS · 2026Article
- Mitochondrial drivers of stem cell aging and inflammaging.npj aging · 2026Review
- Glutaminase 1 in Vascular Disease: Linking Metabolic Reprogramming to Atherosclerosis Progression and Stability.Journal of cardiovascular translational research · 2026Review
- Hyperglutaminolysis drives senescence and aging through arginine-mTORC1 axis activation.Signal transduction and targeted therapy · 2026Article
- Article
- Effects of glutaminase 1 inhibitor on rotator cuff derived cells: a preliminary report in 12 patients.BMC musculoskeletal disorders · 2025Article
- D-2HG Inhibits Glutamine Synthetase Activity and Induces Senescence in IDH-Mutant Gliomas.Aging and disease · 2025Article
- Mitochondrial-encoded peptide MOTS-c prevents pancreatic islet cell senescence to delay diabetes.Experimental & molecular medicine · 2025Article
- Phase separation in mitochondrial fate and mitochondrial diseases.Proceedings of the National Academy of Sciences of the United States of America · 2025Review
- Update of cellular senescence in kidney fibrosis: from mechanism to potential interventions.Frontiers of medicine · 2025Review
- Senolysis by GLS1 Inhibition Ameliorates Kidney Aging by Inducing Excessive mPTP Opening Through MFN1.The journals of gerontology. Series A, Biological sciences and medical sciences · 2025Article
- SMAP3-ID for Identification of Endogenous Protein-Protein Interactions Reveals Regulation of Mitochondrial Activity by Lamins.JACS Au · 2025Article
- Leflunomide-Induced Weight Loss: Involvement of DAHPS Activity and Synthesis of Aromatic Amino Acids.Metabolites · 2024Article
- Glutaminolysis is associated with mitochondrial pathway activation and can be therapeutically targeted in glioblastoma.Cancer & metabolism · 2024Article
- Imbalance of early-life vitamin D intake targets ROS-mediated crosstalk between mitochondrial dysfunction and differentiation potential of MSCs associated the later obesity.Stem cell research & therapy · 2024Article
- Mitochondria, Autophagy and Inflammation: Interconnected in Aging.Cell biochemistry and biophysics · 2024Review
- Ovarian aging: energy metabolism of oocytes.Journal of ovarian research · 2024Review
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial dysfunction, a hallmark of aging, has been associated with the onset of aging phenotypes and age-related diseases. Here, we report that impaired mitochondrial function is associated with increased glutamine catabolism in senescent human mesenchymal stem cells (MSCs) and myofibroblasts derived from patients suffering from Hutchinson-Gilford progeria syndrome. Increased glutaminase (GLS1) activity accompanied by loss of urea transporter SLC14A1 induces urea accumulation, mitochondrial dysfunction, and DNA damage. Conversely, blocking GLS1 activity restores mitochondrial function and leads to amelioration of aging hallmarks. Interestingly, GLS1 expression is regulated through the JNK pathway, as demonstrated by chemical and genetic inhibition. In agreement with our in vitro findings, tissues isolated from aged or progeria mice display increased urea accumulation and GLS1 activity, concomitant with declined mitochondrial function. Inhibition of glutaminolysis in progeria mice improves mitochondrial respiratory chain activity, suggesting that targeting glutaminolysis may be a promising strategy for restoring age-associated loss of mitochondrial function.
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Registered trials
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.