ArticleNature communications2020
Senolytics prevent mt-DNA-induced inflammation and promote the survival of aged organs following transplantation.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers.
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Who cites it
122 citing papers in PubMed, 190 citations in OpenAlex.
- Mechanistic reprogramming of the mtDNA-cGAS-STING axis in cellular senescence: from mitochondrial homeostatic disruption to inflammatory and immune outcomes.Biogerontology · 2026Review
- Toll-like receptor 9-overexpressing red blood cell biomimetic microbubbles adsorb cell-free DNA to relieve steatotic liver ischemia-reperfusion injury.Materials today. Bio · 2026Article
- Transplanted hearts assimilate the recipient's biological age.bioRxiv : the preprint server for biology · 2026Article
- Closing the gap in aging science: unlocking the potential of nanoparticles in senescence therapy.Biogerontology · 2026Review
- The Yin and Yang of cellular senescence in ischemia-induced myocardial injury.Trends in cardiovascular medicine · 2026Review
- Molecular mechanisms and recent advances in cellular senescence.Cell & bioscience · 2026Review
- Review
- Cell-Free DNA-Based Theranostics for Inflammatory Disorders.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Mitochondrial regulation of cellular senescence heterogeneity.Frontiers in cell and developmental biology · 2026Review
- Cellular Senescence, Inflammaging and Cardiovascular Disease.Immunological reviews · 2026Review
- Targeting immunometabolism in cancer through pharmacological and lifestyle interventions.PLoS biology · 2026Review
- Beyond a Biomarker: Investigations of a Proinflammatory Role for Cell-Free DNA in Liver Transplant Ischemia and Reperfusion.Transplant international : official journal of the European Society for Organ Transplantation · 2026Article
- Therapeutic priming of liver regeneration: from mechanisms toFrontiers in transplantation · 2026Review
- Oral microbiome-SASP-aging axis: mechanisms and targeted intervention strategies for age-related diseases.Journal of oral microbiology · 2026Review
- Integrating senotherapeutics into transplantation: liver reconditioning in an aging donor pool.Transplant international : official journal of the European Society for Organ Transplantation · 2026Review
- Mitochondrial DNA efflux as a potential amplifier of systemic inflammatory network rewiring in heart failure with preserved ejection fraction.Frontiers in immunology · 2026Review
- Senotherapeutics for metabolic disease and diabetic complications.Journal of internal medicine · 2026Review
- Donor-recipient age mismatch and outcomes in liver transplantation: A scientific registry of transplant recipients database analysis.World journal of transplantation · 2025Article
- The promise of organ rejuvenation to overcome the shortage in organ transplantation.Nature communications · 2025Review
- Endothelial senescent-cell-specific clearance alleviates metabolic dysfunction in obese mice.Cell metabolism · 2025Article
62 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors at 7 institutions in 4 countries.
Funding
Abstract
Older organs represent an untapped potential to close the gap between demand and supply in organ transplantation but are associated with age-specific responses to injury and increased immunogenicity, thereby aggravating transplant outcomes. Here we show that cell-free mitochondrial DNA (cf-mt-DNA) released by senescent cells accumulates with aging and augments immunogenicity. Ischemia reperfusion injury induces a systemic increase of cf-mt-DNA that promotes dendritic cell-mediated, age-specific inflammatory responses. Comparable events are observed clinically, with the levels of cf-mt-DNA elevated in older deceased organ donors, and with the isolated cf-mt-DNA capable of activating human dendritic cells. In experimental models, treatment of old donor animals with senolytics clear senescent cells and diminish cf-mt-DNA release, thereby dampening age-specific immune responses and prolonging the survival of old cardiac allografts comparable to young donor organs. Collectively, we identify accumulating cf-mt-DNA as a key factor in inflamm-aging and present senolytics as a potential approach to improve transplant outcomes and availability.
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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.