Evidence map›Paper›PMID 41624249›Full record

ReviewMedComm2026

Oxidative Stress: Molecular Mechanisms, Diseases, and Therapeutic Targets.

Yi Qin, Chen Qian, Wenhao Li, Qihan Wang, Qifeng Sheng, Zheqing Chen, Wei Zhang, Wenming Li, Gaoran Ge, Zhanjun Yan and 1 more

Abstract readReview
In one paragraph

Review in MedComm, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. International journal of molecular sciences · 2026
    Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Oxidative Stress in Heat Stress Nephropathy: Crosstalk.Oxidative medicine and cellular longevity · 2026
    Review
  12. Article
  13. 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

11 authors.

Yi QinDepartment of Orthopedics The First Affiliated Hospital of Soochow University, Soochow University Suzhou China.
Chen QianDepartment of Orthopedics The First Affiliated Hospital of Soochow University, Soochow University Suzhou China.
Wenhao LiDepartment of Orthopedics The First Affiliated Hospital of Soochow University, Soochow University Suzhou China.
Qihan WangDepartment of Orthopedics The First Affiliated Hospital of Soochow University, Soochow University Suzhou China.
Qifeng ShengDepartment of Orthopedics The First Affiliated Hospital of Soochow University, Soochow University Suzhou China.
Zheqing ChenDepartment of Orthopedics The First Affiliated Hospital of Soochow University, Soochow University Suzhou China.
Wei ZhangDepartment of Orthopedics The First Affiliated Hospital of Soochow University, Soochow University Suzhou China.
Wenming LiDepartment of Orthopedics The First Affiliated Hospital of Soochow University, Soochow University Suzhou China.
Gaoran GeDepartment of Orthopedics The First Affiliated Hospital of Soochow University, Soochow University Suzhou China.
Zhanjun YanDepartment of Orthopedics Suzhou Ninth Hospital Affiliated to Soochow University Suzhou China.
Dechun GengDepartment of Orthopedics The First Affiliated Hospital of Soochow University, Soochow University Suzhou China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although the physiological level of reactive oxygen species (ROS) is crucial for governing life processes through redox signaling, the excessive accumulation of ROS can contribute to biomolecular damage and pathological state, namely, oxidative stress. This review systematically summarizes the molecular mechanisms underlying the dynamic equilibrium of cellular redox state, including the intracellular sources of ROS and the multilayered antioxidant defense network. When ROS production exceeds the regulatory limits of the antioxidant system, excessive ROS will act on a series of molecular targets and participate in the pathogenesis of diseases. Therapeutic targeting of the redox balance is regarded as an effective strategy for treating oxidative stress-related diseases, such as supplementation of direct antioxidants and enhancement of endogenous antioxidant defense network. Nevertheless, clinical trials that attempt to delay the onset or progression of such diseases are mostly negative. This review discusses the challenges encountered in the clinical application of antioxidant therapy and highlights the opportunities brought by novel technologies such as intelligent drug delivery system and personalized medicine. By adopting these new technologies, it is expected to overcome the limitations of traditional antioxidant therapy.

Indexed as

oxidative damageoxidative stressreactive oxygen speciesredox signalingtherapeutic targets

Identifiers

PMID41624249
PMCPMC12856066

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.