Evidence map›Paper›PMID 36980220›Full record

ReviewCells2023

The Tobacco Smoke Component, Acrolein, as a Major Culprit in Lung Diseases and Respiratory Cancers: Molecular Mechanisms of Acrolein Cytotoxic Activity.

Pawel Hikisz, Damian Jacenik

Open access · goldFull text readReview
In one paragraph

Review in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
13.2field-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

33 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Mutagenicity and Repair of Acrolein Adduct to Cytosine.International journal of molecular sciences · 2025
    Article
  8. Article
  9. Article
  10. Smoking and the risk of prostate cancer: a review of risk and disease progression.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2025
    Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Pawel HikiszDepartment of Oncobiology and Epigenetics, Faculty of Biology and Environmental Protection, University of Lodz, ul. Pomorska 141/143, 90-236 Lodz, Poland.
Damian JacenikDepartment of Cytobiochemistry, Faculty of Biology and Environmental Protection, University of Lodz, ul. Pomorska 141/143, 90-236 Lodz, Poland.ORCID 0000-0003-4563-2303
University of Łódź · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acrolein, a highly reactive unsaturated aldehyde, is a ubiquitous environmental pollutant that seriously threatens human health and life. Due to its high reactivity, cytotoxicity and genotoxicity, acrolein is involved in the development of several diseases, including multiple sclerosis, neurodegenerative diseases such as Alzheimer's disease, cardiovascular and respiratory diseases, diabetes mellitus and even the development of cancer. Traditional tobacco smokers and e-cigarette users are particularly exposed to the harmful effects of acrolein. High concentrations of acrolein have been found in both mainstream and side-stream tobacco smoke. Acrolein is considered one of cigarette smoke's most toxic and harmful components. Chronic exposure to acrolein through cigarette smoke has been linked to the development of asthma, acute lung injury, chronic obstructive pulmonary disease (COPD) and even respiratory cancers. This review addresses the current state of knowledge on the pathological molecular mechanisms of acrolein in the induction, course and development of lung diseases and cancers in smokers.

Indexed as

Electronic Nicotine Delivery SystemsNeoplasmsPulmonary Disease, Chronic ObstructiveTobacco Smoke PollutionAcroleinHumansLungAcroleinTobacco Smoke Pollutionacroleincell signallingCOPDDNA adductsinflammationlung canceroxidative stressrespiratory toxicitytobacco smokeα,β-unsaturated aldehydes

Identifiers

PMID36980220
PMCPMC10047238
OpenAlexW4324056859

What Socratic holds

Textfull text, public
LicenceCC BY
measurements read20
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.