ArticleScience advances2023
RIPK1 blocks T cell senescence mediated by RIPK3 and caspase-8.
Article in Science advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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The trial behind it
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Who cites it
26 citing papers in PubMed, 45 citations in OpenAlex.
- Necroptosis and the RIPK1-RIPK3-MLKL pathway in chronic kidney disease: mechanisms, crosstalk, and therapeutic opportunities.Renal failure · 2026Review
- Cellular senescence and regulated cell death in cancer: mechanisms, cross-regulatory networks and therapeutic implications.Journal of hematology & oncology · 2026Review
- Impact of Losartan Nanoparticles on Carbon Tetrachloride-induced Cerebellar Injury in Rats: Association with Alterations in RIPK1/RIPK3/MLKL Necroptosis Markers.Molecular neurobiology · 2026Article
- Immunosenescence and Vaccine Efficacy in Aging: Dynamic Interplay of Gut Microbiota and mTOR Signaling Pathways.Aging cell · 2026Review
- IL-15 Plus Thymosin α1 Reduces Senescent Hepatic CD8Journal of gastroenterology and hepatology · 2026Article
- RIPK1 regulates β-cell fate via actions on gene expression and kinase signaling in a mouse model of β-cell self-reactivity.Cell death & disease · 2026Article
- Immune Aging as a Failure of Programmed Cell Death Coordination.International journal of molecular sciences · 2026Review
- Ripk1 is critical for preserving effector regulatory T cells and the suppressive transcriptional program in regulatory T cells.Cell death and differentiation · 2026Article
- Clinical Characteristics of Late-Onset (≥ 65 Years) Ulcerative Colitis: A Single-Center Retrospective Study.Gastroenterology research and practice · 2026Article
- RIPK1 Drives JAK1-STAT3 Signaling to Promote CXCL1-Mediated Neutrophil Recruitment in Sepsis-Induced Lung Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- CD4 T cell therapy counteracts inflammaging and senescence by preserving gut barrier integrity.Science immunology · 2025Article
- Necroptotic and Apoptotic Pathways in Sepsis: A Comparative Analysis of Pediatric and Adult ICU Patients.Biomedicines · 2025Article
- Targeting the RAGE-RIPK1 binding site attenuates diabetes-associated cognitive deficits.Journal of neuroinflammation · 2025Article
- Targeting T-cell Aging to Remodel the Aging Immune System and Revitalize Geriatric Immunotherapy.Aging and disease · 2025Review
- Zα and Zβ Localize ADAR1 to Flipons That Modulate Innate Immunity, Alternative Splicing, and Nonsynonymous RNA Editing.International journal of molecular sciences · 2025Review
- Article
- RIPK1 signaling pathways: implications for autoimmune and neuroinflammatory diseases.Frontiers in immunology · 2025Review
- Serum Level of RIPK1/3 Correlated With the Prognosis in ICU Patients With Acute Ischemic Stroke.Immunity, inflammation and disease · 2024Article
- Senescent T Cells: The Silent Culprit in Acute Myeloid Leukemia Progression?International journal of molecular sciences · 2024Review
- SHP2-Triggered Endothelial Cell Activation Fuels Estradiol-Independent Endometrial Sterile Inflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Receptor-interacting protein kinase 1 (RIPK1) regulates cell death and inflammation. Here, we show that T cell-specific RIPK1 deficiency in mice leads to the premature senescence of T cells and induces various age-related diseases, resulting in premature death. RIPK1 deficiency causes higher basal activation of mTORC1 (mechanistic target of rapamycin complex 1) that drives enhanced cytokine production, induction of senescence-related genes, and increased activation of caspase-3/7, which are restored by inhibition of mTORC1. Critically, normal aged T cells exhibit similar phenotypes and responses. Mechanistically, a combined deficiency of RIPK3 and caspase-8 inhibition restores the impaired proliferative responses; the elevated activation of Akt, mTORC1, extracellular signal-regulated kinase, and caspase-3/7; and the increased expression of senescence-related genes in RIPK1-deficient CD4 T cells. Last, we revealed that the senescent phenotype of RIPK1-deficient and aged CD4 T cells is restored in the normal tissue environment. Thus, we have clarified the function of RIPK3 and caspase-8 in inducing CD4 T cell senescence, which is modulated by environmental signals.
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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.