ReviewFree radical biology & medicine2017
DNA damage related crosstalk between the nucleus and mitochondria.
Review in Free radical biology & medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 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
85 citing papers in PubMed, 151 citations in OpenAlex.
- Dietary riboflavin blocks the cGAS-STING pathway to curb hypoxia-induced hepatic inflammation in sub-adult grass carp (Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2026Article
- Unraveling the link between genomic instability and tumor immune evasion in oral squamous cell carcinoma: Role of CBMN assay and emerging perspectives.Medical oncology (Northwood, London, England) · 2026Review
- Extracellular vesicles: Revolutionizing targeted therapy for ischemic stroke.Acta pharmaceutica Sinica. B · 2026Review
- Endothelial senescence of the vertebral artery in the context of cervical degeneration: biomechanically driven remodeling of the hemodynamic environment.Frontiers in cell and developmental biology · 2026Review
- Organelle-oriented nanomedicines in tumor therapy: Targeting, escaping, or collaborating?Bioactive materials · 2025Review
- Mitochondria-Nuclear Crosstalk: Orchestrating mtDNA Maintenance.Environmental and molecular mutagenesis · 2025Review
- Nuclear Genome-Encoded Mitochondrial OXPHOS Complex I Genes in Female Buffalo Show Tissue-Specific Differences.Molecular biotechnology · 2025Article
- Endometrial Aging and Reproductive Decline: The Central Role of Mitochondrial Dysfunction.International journal of molecular sciences · 2025Review
- DNA damage response regulator ATR licenses PINK1-mediated mitophagy.Nucleic acids research · 2025Article
- Including genetic susceptibility towards Parkinson's disease in NAM-based hazard and risk assessment of pesticides: a semi-systematic review.NAM journal · 2025Review
- NFκB1: a common biomarker linking Alzheimer's and Parkinson's disease pathology.Frontiers in neuroscience · 2025Article
- Immunometabolism and male reproductive function: linking inflammation, oxidative stress, and declining fertility.Frontiers in immunology · 2025Review
- Epigenetic regulation of transcription factors involved in NLRP3 inflammasome and NF-kB signaling pathways.Frontiers in immunology · 2025Review
- Artificial targeting of the NEIL1 DNA glycosylase to the mitochondria.Environmental and molecular mutagenesis · 2024Article
- UV damage induces production of mitochondrial DNA fragments with specific length profiles.Genetics · 2024Article
- Blocking reverse electron transfer-mediated mitochondrial DNA oxidation rescues cells from PANoptosis.Acta pharmacologica Sinica · 2024Article
- Mitochondrial proteome research: the road ahead.Nature reviews. Molecular cell biology · 2024Review
- Alleviating Neurodegenerative Diseases Associated with Mitochondrial Defects by Therapeutic Biomolecules.Current topics in medicinal chemistry · 2024Review
- Systemic Evidence for Mitochondrial Dysfunction in Age-Related Macular Degeneration as Revealed by mtDNA Copy Number Measurements in Peripheral Blood.International journal of molecular sciences · 2023Article
- UV damage induces production of mitochondrial DNA fragments with specific length profiles.bioRxiv : the preprint server for biology · 2023Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The electron transport chain is the primary pathway by which a cell generates energy in the form of ATP. Byproducts of this process produce reactive oxygen species that can cause damage to mitochondrial DNA. If not properly repaired, the accumulation of DNA damage can lead to mitochondrial dysfunction linked to several human disorders including neurodegenerative diseases and cancer. Mitochondria are able to combat oxidative DNA damage via repair mechanisms that are analogous to those found in the nucleus. Of the repair pathways currently reported in the mitochondria, the base excision repair pathway is the most comprehensively described. Proteins that are involved with the maintenance of mtDNA are encoded by nuclear genes and translocate to the mitochondria making signaling between the nucleus and mitochondria imperative. In this review, we discuss the current understanding of mitochondrial DNA repair mechanisms and also highlight the sensors and signaling pathways that mediate crosstalk between the nucleus and mitochondria in the event of mitochondrial stress.
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.