Evidence map›Paper›PMID 37760035›Full record

ReviewAntioxidants (Basel, Switzerland)2023

Cigarette Smoke-Induced Reactive Oxygen Species Formation: A Concise Review.

Yoon-Seok Seo, Jung-Min Park, Jae-Hyeong Kim, Moo-Yeol Lee

Open access · goldAbstract 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 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
14.3field-weighted citation impact, top 1% of its field
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

70 citing papers in PubMed, 93 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Observational
  6. Article
  7. Article
  8. Review
  9. The Oxidative Stress: Origin and Role in Aging and Diseases.Antioxidants (Basel, Switzerland) · 2026
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Antioxidant Peptides fromMarine drugs · 2026
    Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

10 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Yoon-Seok SeoBK21 FOUR Team and Integrated Research Institute for Drug Development, College of Pharmacy, Dongguk University, Goyang-si 10326, Gyeonggi-do, Republic of Korea.
Jung-Min ParkBK21 FOUR Team and Integrated Research Institute for Drug Development, College of Pharmacy, Dongguk University, Goyang-si 10326, Gyeonggi-do, Republic of Korea.
Jae-Hyeong KimBK21 FOUR Team and Integrated Research Institute for Drug Development, College of Pharmacy, Dongguk University, Goyang-si 10326, Gyeonggi-do, Republic of Korea.
Moo-Yeol LeeBK21 FOUR Team and Integrated Research Institute for Drug Development, College of Pharmacy, Dongguk University, Goyang-si 10326, Gyeonggi-do, Republic of Korea.ORCID 0000-0003-4440-8967
Dongguk University · KR

Funding

Dongguk University Research Fund of 2022 S-2022-G0001-00132Ministry of Education BK21 FOUR programMinistry of Food and Drug Safety 21203MFDS318National Research Foundation of Korea 2022R1A2C2007171National Research Foundation of Korea NRF-2018R1A5A2023127
6 · The paper itself

Abstract

Smoking is recognized as a significant risk factor for numerous disorders, including cardiovascular diseases, respiratory conditions, and various forms of cancer. While the exact pathogenic mechanisms continue to be explored, the induction of oxidative stress via the production of excess reactive oxygen species (ROS) is widely accepted as a primary molecular event that predisposes individuals to these smoking-related ailments. This review focused on how cigarette smoke (CS) promotes ROS formation rather than the pathophysiological repercussions of ROS and oxidative stress. A comprehensive analysis of existing studies revealed the following key ways through which CS imposes ROS burden on biological systems: (1) ROS, as well as radicals, are intrinsically present in CS, (2) CS constituents generate ROS through chemical reactions with biomolecules, (3) CS stimulates cellular ROS sources to enhance production, and (4) CS disrupts the antioxidant system, aggravating the ROS generation and its functions. While the evidence supporting these mechanisms is chiefly based on in vitro and animal studies, the direct clinical relevance remains to be fully elucidated. Nevertheless, this understanding is fundamental for deciphering molecular events leading to oxidative stress and for developing intervention strategies to counter CS-induced oxidative stress.

Indexed as

cigarette smokeNADPH oxidaseoxidative stressreactive oxygen speciessmoking

Identifiers

PMID37760035
PMCPMC10525535
OpenAlexW4386524852

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.