ArticlePloS one2022
The mTOR inhibitor Rapamycin protects from premature cellular senescence early after experimental kidney transplantation.
Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 23 citations in OpenAlex.
- T-Cell Remodeling in Renal Fibrosis: From Acute Injury to Chronic Kidney Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Multi-Omics Analysis of PBMCs Revealed Distinct Biological Differences Between Hemodialysis and Peritoneal Dialysis.International journal of molecular sciences · 2026Article
- Integrative Approaches to Treating Cellular Senescence in Kidney Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Integrating senotherapeutics into transplantation: liver reconditioning in an aging donor pool.Transplant international : official journal of the European Society for Organ Transplantation · 2026Review
- Lens epithelial cells senescence in cataract pathogenesis and emerging therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
- Viral infections in solid organ transplant recipients: immunological principles and intervention strategies.American journal of translational research · 2026Review
- Targeting Aging and Diseases Associated with Ferroptosis and Senescence Through Modulation of Iron, Oxidative Stress and Lipid Peroxidation.Antioxidants (Basel, Switzerland) · 2025Review
- Senotherapeutics for Brain Aging Management.Neurology international · 2025Review
- The promise of organ rejuvenation to overcome the shortage in organ transplantation.Nature communications · 2025Review
- Article
- Cellular senescence in renal ischemia-reperfusion injury.Chinese medical journal · 2025Review
- Understanding and targeting senescence in kidney disease.Clinical kidney journal · 2025Review
- Update of cellular senescence in kidney fibrosis: from mechanism to potential interventions.Frontiers of medicine · 2025Review
- Therapeutic approaches targeting aging and cellular senescence in Huntington's disease.CNS neuroscience & therapeutics · 2024Review
- Long-term outcomes in rapamycin on renal allograft function: a 30-year follow-up from a single-center experience.BMC nephrology · 2024Article
- Navigating the Neuroimmunomodulation Frontier: Pioneering Approaches and Promising Horizons-A Comprehensive Review.International journal of molecular sciences · 2024Review
- mTOR and SGLT-2 Inhibitors: Their Synergistic Effect on Age-Related Processes.International journal of molecular sciences · 2024Review
- Article
- Translating Senotherapeutic Interventions into the Clinic with Emerging Proteomic Technologies.Biology · 2023Review
- Cellular Senescence and Frailty in Transplantation.Current transplantation reports · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interstitial fibrosis and tubular atrophy, a major cause of kidney allograft dysfunction, has been linked to premature cellular senescence. The mTOR inhibitor Rapamycin protects from senescence in experimental models, but its antiproliferative properties have raised concern early after transplantation particularly at higher doses. Its effect on senescence has not been studied in kidney transplantation, yet. Rapamycin was applied to a rat kidney transplantation model (3 mg/kg bodyweight loading dose, 1.5 mg/kg bodyweight daily dose) for 7 days. Low Rapamycin trough levels (2.1-6.8 ng/mL) prevented the accumulation of p16INK4a positive cells in tubules, interstitium, and glomerula. Expression of the cytokines MCP-1, IL-1β, and TNF-α, defining the proinflammatory senescence-associated secretory phenotype, was abrogated. Infiltration with monocytes/macrophages and CD8+ T-lymphocytes was reduced and tubular function was preserved by Rapamycin. Inhibition of mTOR was not associated with impaired structural recovery, higher glucose levels, or weight loss. mTOR inhibition with low-dose Rapamycin in the immediate posttransplant period protected from premature cellular senescence without negative effects on structural and functional recovery from preservation/reperfusion damage, glucose homeostasis, and growth in a rat kidney transplantation model. Reduced senescence might maintain the renal regenerative capacity rendering resilience to future injuries resulting in protection from interstitial fibrosis and tubular atrophy.
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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 Socratic graph.