ArticleAmerican journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons2022
IFI16-STING-NF-κB signaling controls exogenous mitochondrion-induced endothelial activation.
Article in American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Needle-warming moxibustion alleviates pain in rats with cervical spondylotic radiculopathy by modulating the NF-κB/ROS/NLRP3 pathway.Frontiers in aging neuroscience · 2026Article
- Mitochondrial DNA-driven intercellular communication networks in post-infarction ventricular remodeling: the three-threshold model of cGAS-STING activation.Frontiers in immunology · 2026Review
- PRRs-Dependent and Independent Mechanisms of STING Signaling in Inflammatory and Autoimmune Diseases.Biomedicines · 2025Review
- IFI16 Induced by p53 Activates the NF-κB Pathway to Counteract Cisplatin-Induced Apoptosis in Cervical Cancer Cells.Journal of cellular and molecular medicine · 2025Article
- Rapamycin Prevents Expansion of Costimulation Blockade-resistant CD8+ Alloreactive Memory Cells following Depletional Induction in Renal Transplant Recipients.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Article
- Review
- The role of IFI16 in regulating PANoptosis and implication in heart diseases.Cell death discovery · 2024Review
- CD62E- and ROS-Responsive ETS Improves Cartilage Repair by Inhibiting Endothelial Cell Activation through OPA1-Mediated Mitochondrial Homeostasis.Biomaterials research · 2024Article
- cGAS-STING pathway in ischemia-reperfusion injury: a potential target to improve transplantation outcomes.Frontiers in immunology · 2023Review
- Link between sterile inflammation and cardiovascular diseases: Focus on cGAS-STING pathway in the pathogenesis and therapeutic prospect.Frontiers in cardiovascular medicine · 2022Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondria released from injured cells activate endothelial cells (ECs), fostering inflammatory processes, including allograft rejection. The stimulator of interferon genes (STING) senses endogenous mitochondrial DNA, triggering innate immune activation via NF-κB signaling. Here, we show that exogenous mitochondria exposure induces EC STING-NF-κB activation, promoting EC/effector memory T cell adhesion, which is abrogated by NF-κB and STING inhibitors. STING activation in mitochondrion-activated ECs is independent of canonical cGMP-AMP synthetase sensing/signaling, but rather is mediated by interferon gamma-inducible factor 16 (IFI16) and can be inhibited by IFI16 inhibition. Internalized mitochondria undergo mitofusion and STING-dependent mitophagy, leading to selective sequestration of internalized mitochondria. The exposure of donor hearts to exogenous mitochondria activates murine heart ECs in vivo. Collectively, our results suggest that IFI16-STING-NF-κB signaling regulates exogenous mitochondrion-induced EC activation and mitophagy, and exogenous mitochondria foster T cell-mediated CoBRR. These data suggest a novel, donor-directed, therapeutic approach toward mitigating perioperative allograft immunogenicity.
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Registered trials
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