ReviewFrontiers in immunology2021
Circulating Mitochondrial DNA Stimulates Innate Immune Signaling Pathways to Mediate Acute Kidney Injury.
Review in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
40 citing papers in PubMed, 54 citations in OpenAlex.
- Mitochondrial DNA leakage in oocytes activates cGAS-STING signaling to drive ovarian aging.Nature aging · 2026Article
- Cardiometabolic Aging Driven by Multi-Organ Crosstalk: Mechanisms and Therapeutic Strategies.International journal of molecular sciences · 2026Review
- Mitochondrial Dysfunction at the Intersection of CKM Syndrome: Molecular Mechanisms and Path-to-Target Therapies.International journal of molecular sciences · 2026Review
- Mitochondrial Dysfunction in Acute Kidney Injury: Intersections Between Chemotherapy and Novel Cancer Immunotherapies.Biomolecules · 2026Review
- Mitochondrial metabolic reprogramming, quality control, and intercellular transfer in regulating macrophage plasticity.Frontiers in physiology · 2026Review
- Novel insights of ferroptosis in atherosclerosis progression.Frontiers in cell and developmental biology · 2026Review
- Liraglutide and renal mitochondrial homeostasis: targeting the "metabolism-inflammation-lithogenesis" axis in metabolic syndrome.Frontiers in pharmacology · 2026Review
- Mitochondrial homeostasis and aging: the mtDNA-cGAS-STING axis.Frontiers in immunology · 2026Review
- When Mitochondria Falter, the Barrier Fails: Mechanisms of Inner Blood-Retinal Barrier (iBRB) Injury and Opportunities for Mitochondria-Targeted Repair.International journal of molecular sciences · 2025Review
- Cell-free DNA in sepsis: from molecular insights to clinical management.Military Medical Research · 2025Review
- The emerging roles of platelet-derived extracellular vesicles in disease.Annals of medicine · 2025Review
- Revealing Cell-Free Mitochondrial DNA Breakage Patterns as Novel Biomarkers for Sepsis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Kidneys on the Frontline: Nephrologists Tackling the Wilds of Acute Kidney Injury in Trauma Patients-From Pathophysiology to Early Biomarkers.Diagnostics (Basel, Switzerland) · 2025Review
- Progress in targeting the NLRP3 signaling pathway for inflammatory bowel disease (Review).Molecular medicine reports · 2025Review
- Damage-associated molecular patterns (DAMPs) in diseases: implications for therapy.Molecular biomedicine · 2025Review
- From sting to STING: role of inflammation in wasp sting induced AKI - a narrative review.BMC nephrology · 2025Review
- The role of mitochondrial reactive oxygen species in initiating mitochondrial damage and inflammation in wasp-venom-induced acute kidney injury.Journal of toxicologic pathology · 2025Article
- Research progress on damage-associated molecular patterns in acute kidney injury.Frontiers in immunology · 2025Review
- Cell-free mitochondrial DNA as a pro-inflammatory agent in blood circulation: mechanisms, therapeutic implications, and clinical challenges in immune dysregulation.Frontiers in immunology · 2025Review
- Role of damage-associated molecular patterns in the pathogenesis and therapeutics of traumatic brain injury.Burns & trauma · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction is increasingly considered as a critical contributor to the occurrence and progression of acute kidney injury (AKI). However, the mechanisms by which damaged mitochondria mediate AKI progression are multifactorial and complicated. Mitochondrial DNA (mtDNA) released from damaged mitochondria could serve as a danger-associated molecular pattern (DAMP) and activate the innate immune system through STING, TLR9, NLRP3, and some other adaptors, and further mediate tubular cell inflammation and apoptosis. Accumulating evidence has demonstrated the important role of circulating mtDNA and its related pathways in the progression of AKI, and regulating the proteins involved in these pathways may be an effective strategy to reduce renal tubular injury and alleviate AKI. Here, we aim to provide a comprehensive overview of recent studies on mtDNA-mediated renal pathological events to provide new insights in the setting of AKI.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.