Evidence map›Paper›PMID 37107309›Full record

ReviewAntioxidants (Basel, Switzerland)2023

Targeting Mitochondrial Oxidative Stress as a Strategy to Treat Aging and Age-Related Diseases.

Yun Haeng Lee, Myeong Uk Kuk, Moon Kyoung So, Eun Seon Song, Haneur Lee, Soon Kil Ahn, Hyung Wook Kwon, Joon Tae Park, Sang Chul Park

Abstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing 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

38 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
  5. 2-Methoxystypandrone fromAntioxidants (Basel, Switzerland) · 2026
    Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Frontiers in aging · 2026
    Article
  11. Article
  12. Article
  13. ε-Viniferin Rejuvenates Senescence viaPharmaceuticals (Basel, Switzerland) · 2025
    Article
  14. Review
  15. Review
  16. Article
  17. Epigallocatechin Gallate inPharmaceuticals (Basel, Switzerland) · 2025
    Article
  18. Article
  19. Article
  20. Article
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

9 authors.

Yun Haeng LeeDivision of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon 22012, Republic of Korea.
Myeong Uk KukDivision of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon 22012, Republic of Korea.
Moon Kyoung SoDivision of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon 22012, Republic of Korea.
Eun Seon SongDivision of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon 22012, Republic of Korea.
Haneur LeeDivision of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon 22012, Republic of Korea.
Soon Kil AhnDivision of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon 22012, Republic of Korea.
Hyung Wook KwonDivision of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon 22012, Republic of Korea.ORCID 0000-0001-9340-7974
Joon Tae ParkDivision of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon 22012, Republic of Korea.ORCID 0000-0003-2396-9108
Sang Chul ParkThe Future Life & Society Research Center, Chonnam National University, Gwangju 61186, Republic of Korea.

Funding

National Research Foundation of Korea 2020R1A6A1A0304195411National Research Foundation of Korea NRF-2021R1A2C1004298
6 · The paper itself

Abstract

Mitochondria are one of the organelles undergoing rapid alteration during the senescence process. Senescent cells show an increase in mitochondrial size, which is attributed to the accumulation of defective mitochondria, which causes mitochondrial oxidative stress. Defective mitochondria are also targets of mitochondrial oxidative stress, and the vicious cycle between defective mitochondria and mitochondrial oxidative stress contributes to the onset and development of aging and age-related diseases. Based on the findings, strategies to reduce mitochondrial oxidative stress have been suggested for the effective treatment of aging and age-related diseases. In this article, we discuss mitochondrial alterations and the consequent increase in mitochondrial oxidative stress. Then, the causal role of mitochondrial oxidative stress on aging is investigated by examining how aging and age-related diseases are exacerbated by induced stress. Furthermore, we assess the importance of targeting mitochondrial oxidative stress for the regulation of aging and suggest different therapeutic strategies to reduce mitochondrial oxidative stress. Therefore, this review will not only shed light on a new perspective on the role of mitochondrial oxidative stress in aging but also provide effective therapeutic strategies for the treatment of aging and age-related diseases through the regulation of mitochondrial oxidative stress.

Indexed as

aging controlmitochondriamitochondrial oxidative stressROS

Identifiers

PMID37107309
PMCPMC10136354

What OpenQuestion 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 OpenQuestion graph.