Evidence map›Paper›PMID 41303849›Full record

ReviewMedicina (Kaunas, Lithuania)2025

Cellular and Molecular Mechanisms of Oxidative DNA Damage and Repair.

Adnan Ayna, Cuneyt Caglayan, Seyithan Taysi

Abstract readReview
In one paragraph

Review in Medicina (Kaunas, Lithuania), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Adnan AynaDepartment of Chemistry, Faculty of Science and Literature, Bingol University, 12000 Bingol, Turkey.ORCID 0000-0001-6801-6242
Cuneyt CaglayanDepartment of Medical Biochemistry, Faculty of Medicine, Bilecik Seyh Edebali University, 11230 Bilecik, Turkey.ORCID 0000-0001-5608-554X
Seyithan TaysiDepartment of Medical Biochemistry, Faculty of Medicine, Gaziantep University, 27410 Gaziantep, Turkey.ORCID 0000-0003-1251-3148

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA is continuously exposed to endogenous and exogenous factors that induce oxidative modifications leading to mutations and genomic instability. Oxidative DNA damage plays a dual role, contributing to physiological signaling at low levels while promoting mutagenesis, carcinogenesis and degenerative diseases when unpaired. Among various lesions, an oxidized base, such as 8-oxo-2'-deoxyguanosine (8-oxodG), is one of the major biomarkers of oxidative stress and genomic damage. Cells have evolved sophisticated repair processes, including base excision repair (BER), nucleotide excision repair (NER), and mismatch repair (MMR), to maintain genomic integrity. Dysregulation or polymorphism of these repair genes has been linked with cancer, neurologic, and cardiovascular disorders. This review discusses an overview of what is presently known concerning oxidative DNA damage and repair mechanisms, particularly emphasizing their molecular players, signaling routes, and human disease implications. It further refers to the latest advances in CRISPR-based technologies and multi-omics approaches that are redefining our understanding of DNA damage response (DDR) networks and creating new frontiers for therapeutic interventions.

Indexed as

DNA DamageDNA RepairOxidative StressHumanscell damageDNA damageDNA repair mechanismsfree radicalsstresses

Identifiers

PMID41303849
PMCPMC12654592

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.