ReviewJournal of inflammation research2025
Novel Perspectives in Hepatic Ischemia-Reperfusion Injury: The cGAS-STING Pathway.
Review in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- From mitochondria to innate immunity: The mtDNA-driven cGAS/STING-NLRP3 cascade and its therapeutic implications in neurodegenerative diseases (Review).Experimental and therapeutic medicine · 2026Review
- Dynamic regulation and targeted intervention of neutrophils in hepatic ischemia‑reperfusion injury (Review).International journal of molecular medicine · 2026Review
- Mitochondrial DNA regulation of hepatic ischemia-reperfusion injury and intervention strategies.Journal of translational medicine · 2026Review
- Mitochondrial DNA as a driver of inflammation via the cGAS-STING pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Interactions between neutrophil extracellular traps and macrophages: the key to inflammatory diseases.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In hepatic ischemia-reperfusion injury (HIRI), the cGAS-STING pathway serves as a central regulatory hub by sensing aberrant mitochondrial DNA (mtDNA) release. Ischemia-reperfusion triggers mtDNA leakage through mechanisms including mitochondrial permeability transition pore (mPTP) opening, voltage-dependent anion channel (VDAC) oligomerization, and excessive fission. Cytosolic mtDNA activates cyclic GMP-AMP synthase (cGAS), catalyzing the synthesis of cGAMP, which stimulates stimulator of interferon genes (STING) oligomerization and translocation. This activates the TBK1-IRF3/NF-κB axis, driving expression of type I interferons (IFN-I) and pro-inflammatory cytokines, thereby amplifying neutrophil infiltration, macrophage pyroptosis, and hepatocyte apoptosis. The pathway bidirectionally interacts with oxidative stress and mitophagy, exhibiting cell-type specificity: in hepatocytes, cGAS promotes protective STING-independent autophagy, whereas in macrophages, STING drives inflammatory activation. Targeted inhibition of cGAS-STING signaling and mitochondrial stabilization represent promising therapeutic strategies.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.