ReviewOxidative medicine and cellular longevity2021
Mitochondrial DNA-Mediated Inflammation in Acute Kidney Injury and Chronic Kidney Disease.
Review in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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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Who cites it
28 citing papers in PubMed, 50 citations in OpenAlex.
- Nucleic acid sensing pathways in kidney disease development.Nature reviews. Nephrology · 2026Review
- Oxidative Stress and Mitochondrial Dysfunction in Chronic Kidney Disease: From Molecular Mechanisms to Biomarkers and Targeted Therapies.Antioxidants (Basel, Switzerland) · 2026Review
- Targeting PSAT1 in diabetic kidney disease: a ferroptosis-driven strategy for precision therapy.Molecular and cellular biochemistry · 2026Article
- cGAS-STING pathway in innate immunity and its cell-specific role in kidney diseases.Frontiers in immunology · 2026Review
- Mitochondrial DNA copy number reduction viaEpigenomics · 2026Article
- Kidneys on the Frontline: Nephrologists Tackling the Wilds of Acute Kidney Injury in Trauma Patients-From Pathophysiology to Early Biomarkers.Diagnostics (Basel, Switzerland) · 2025Review
- RGD hydrogel-loaded ADSC extracellular vesicles mitigate uranium-induced renal injury via TLR4/NF-κB pathway inhibition.Journal of nanobiotechnology · 2025Article
- Vascularization, Innervation, and Inflammation: Pathways Connecting the Heart-Brain Axis and Implications in a Clinical Setting.Biomedicines · 2025Review
- Blood-derived mitochondrial DNA copy number is associated with Alzheimer disease, Alzheimer-related biomarkers and serum metabolites.Alzheimer's research & therapy · 2024Article
- The cGAS-STING pathway: a therapeutic target in diabetes and its complications.Burns & trauma · 2024Review
- The effects of cGAS-STING inhibition in liver disease, kidney disease, and cellular senescence.Frontiers in immunology · 2024Review
- Mitochondrial DNA Variants at Low-Level Heteroplasmy and Decreased Copy Numbers in Chronic Kidney Disease (CKD) Tissues with Kidney Cancer.International journal of molecular sciences · 2023Article
- STING deficiency protects against wasp venom-induced acute kidney injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Autophagy and mitophagy: physiological implications in kidney inflammation and diseases.American journal of physiology. Renal physiology · 2023Review
- The Multi-Faceted Nature of Renalase for Mitochondrial Dysfunction Improvement in Cardiac Disease.Cells · 2023Review
- Mitochondrial Oxidative Metabolism: An Emerging Therapeutic Target to Improve CKD Outcomes.Biomedicines · 2023Review
- Molecular mechanisms of ferroptosis and relevance to inflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- The Activation of cGAS-STING in Acute Kidney Injury.Journal of inflammation research · 2023Review
- Pharmacological functions of salidroside in renal diseases: facts and perspectives.Frontiers in pharmacology · 2023Review
- The nuclear factor kappa B signaling pathway is a master regulator of renal fibrosis.Frontiers in pharmacology · 2023Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The integrity and function of mitochondria are essential for normal kidney physiology. Mitochondrial DNA (mtDNA) has been widely a concern in recent years because its abnormalities may result in disruption of aerobic respiration, cellular dysfunction, and even cell death. Particularly, aberrant mtDNA copy number (mtDNA-CN) is associated with the development of acute kidney injury and chronic kidney disease, and urinary mtDNA-CN shows the potential to be a promising indicator for clinical diagnosis and evaluation of kidney function. Several lines of evidence suggest that mtDNA may also trigger innate immunity, leading to kidney inflammation and fibrosis. In mechanism, mtDNA can be released into the cytoplasm under cell stress and recognized by multiple DNA-sensing mechanisms, including Toll-like receptor 9 (TLR9), cytosolic cGAS-stimulator of interferon genes (STING) signaling, and inflammasome activation, which then mediate downstream inflammatory cascades. In this review, we summarize the characteristics of these mtDNA-sensing pathways mediating inflammatory responses and their role in the pathogenesis of acute kidney injury, nondiabetic chronic kidney disease, and diabetic kidney disease. In addition, we highlight targeting of mtDNA-mediated inflammatory pathways as a novel therapeutic target for these kidney diseases.
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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.