Evidence map›Paper›PMID 38955925›Full record

ReviewCell biochemistry and biophysics2024

Mechanisms of Bleomycin-induced Lung Fibrosis: A Review of Therapeutic Targets and Approaches.

Shaimaa M Mohammed, Haider Falih Shamikh Al-Saedi, Amjed Qasim Mohammed, Ahmed Ali Amir, Usama Kadem Radi, Ruaa Sattar, Irfan Ahmad, Montather F Ramadan, Mohammad Y Alshahrani, Halah Majeed Balasim and 1 more

Abstract readReview
PubMed Publisher
In one paragraph

Review in Cell biochemistry and biophysics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. The role of IL-11 in chronic diseases.Frontiers in immunology · 2026
    Review
  9. Review
  10. Review
  11. FAPI TracerPharmaceuticals (Basel, Switzerland) · 2025
    Article
  12. Review
  13. Article
  14. Article
  15. [Pathophysiology of fibrosis: inflammatory vs. non-inflammatory].Innere Medizin (Heidelberg, Germany) · 2025
    Review
  16. Article
  17. 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

11 authors.

Shaimaa M MohammedDepartment of Pharmacy, Al- Mustaqbal University College, 51001, Hilla, Babylon, Iraq.
Haider Falih Shamikh Al-SaediFaculty of pharmacy, Department of pharmaceutic, University of Al-Ameed, Karbala, Iraq.
Amjed Qasim MohammedAl-Manara College for Medical Sciences, Amarah, Maysan, Iraq.
Ahmed Ali AmirDepartment of Medical Laboratories Technology, Al-Nisour University College, Baghdad, Iraq.
Usama Kadem RadiCollege of Pharmacy, National University of Science and Technology, Nasiriyah, Dhi Qar, Iraq.
Ruaa SattarAl-Hadi University College, Baghdad, 10011, Iraq.
Irfan AhmadDepartment of Clinical Laboratory Sciences, College of Applied Medical Sciences, King Khalid University, Abha, Saudi Arabia.
Montather F RamadanCollege of Dentistry, Al-Ayen University, Nasiriyah, Thi-Qar, Iraq.
Mohammad Y AlshahraniDepartment of Clinical Laboratory Sciences, College of Applied Medical Sciences, King Khalid University, Abha, Saudi Arabia. moyahya@kku.edu.sa.
Halah Majeed BalasimDepartment of Medical Laboratory Technologies, Al Rafidain University College, Bagdad, Iraq.
Ahmed AlawadiCollege of technical engineering, the Islamic University, Najaf, Iraq.

Funding

Deanship of Scientific Research, King Khalid University RGP.02/260/44
6 · The paper itself

Abstract

Pulmonary toxicity is a serious side effect of some specific anticancer drugs. Bleomycin is a well-known anticancer drug that triggers severe reactions in the lungs. It is an approved drug that may be prescribed for the treatment of testicular cancers, Hodgkin's and non-Hodgkin's lymphomas, ovarian cancer, head and neck cancers, and cervical cancer. A large number of experimental studies and clinical findings show that bleomycin can concentrate in lung tissue, leading to massive oxidative stress, alveolar epithelial cell death, the proliferation of fibroblasts, and finally the infiltration of immune cells. Chronic release of pro-inflammatory and pro-fibrotic molecules by immune cells and fibroblasts leads to pneumonitis and fibrosis. Both fibrosis and pneumonitis are serious concerns for patients who receive bleomycin and may lead to death. Therefore, the management of lung toxicity following cancer therapy with bleomycin is a critical issue. This review explains the cellular and molecular mechanisms of pulmonary injury following treatment with bleomycin. Furthermore, we review therapeutic targets and possible promising strategies for ameliorating bleomycin-induced lung injury.

Indexed as

BleomycinPulmonary FibrosisAnimalsAntibiotics, AntineoplasticHumansLungOxidative StressAntibiotics, AntineoplasticBleomycinAlveolar Epithelial CellsBleomycinFibroblastFibrosisLungPulmonary Fibrosis

Identifiers

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Registered trials

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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.