Evidence map›Paper›PMID 36835428›Full record

ReviewInternational journal of molecular sciences2023

Fibrosis: Types, Effects, Markers, Mechanisms for Disease Progression, and Its Relation with Oxidative Stress, Immunity, and Inflammation.

Samar A Antar, Nada A Ashour, Mohamed E Marawan, Ahmed A Al-Karmalawy

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 198 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
198citing papers in PubMed, 4 pooled it
77.6field-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

198 citing papers in PubMed, 4 syntheses or guidelines pooled it, 300 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. The efficacy and safety ofFrontiers in pharmacology · 2024
    Pooled it
  5. Review
  6. Thromborepair: the tissue repair partner to thromboinflammation.Blood vessels, thrombosis & hemostasis · 2026
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Tanshinone IIChinese herbal medicines · 2026
    Article
  20. Review

138 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 3 institutions in 2 countries.

Samar A AntarDepartment of Pharmacology and Biochemistry, Faculty of Pharmacy, Horus University, New Damietta 34518, Damietta, Egypt.ORCID 0000-0002-1223-3579
Nada A AshourDepartment of Clinical Pharmacology and Toxicology, Faculty of Pharmacy, Tanta University, Tanta 31527, Gharbia, Egypt.ORCID 0000-0001-6250-7198
Mohamed E MarawanDepartment of Pharmacology and Biochemistry, Faculty of Pharmacy, Horus University, New Damietta 34518, Damietta, Egypt.
Ahmed A Al-KarmalawyPharmaceutical Chemistry Department, Faculty of Pharmacy, Ahram Canadian University, 6th of October City 12566, Giza, Egypt.ORCID 0000-0002-8173-6073
Damietta University · EGAhram Canadian University · EGTanta University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Most chronic inflammatory illnesses include fibrosis as a pathogenic characteristic. Extracellular matrix (ECM) components build up in excess to cause fibrosis or scarring. The fibrotic process finally results in organ malfunction and death if it is severely progressive. Fibrosis affects nearly all tissues of the body. The fibrosis process is associated with chronic inflammation, metabolic homeostasis, and transforming growth factor-β1 (TGF-β1) signaling, where the balance between the oxidant and antioxidant systems appears to be a key modulator in managing these processes. Virtually every organ system, including the lungs, heart, kidney, and liver, can be affected by fibrosis, which is characterized as an excessive accumulation of connective tissue components. Organ malfunction is frequently caused by fibrotic tissue remodeling, which is also frequently linked to high morbidity and mortality. Up to 45% of all fatalities in the industrialized world are caused by fibrosis, which can damage any organ. Long believed to be persistently progressing and irreversible, fibrosis has now been revealed to be a very dynamic process by preclinical models and clinical studies in a variety of organ systems. The pathways from tissue damage to inflammation, fibrosis, and/or malfunction are the main topics of this review. Furthermore, the fibrosis of different organs with their effects was discussed. Finally, we highlight many of the principal mechanisms of fibrosis. These pathways could be considered as promising targets for the development of potential therapies for a variety of important human diseases.

Indexed as

FibrosisInflammationOxidative StressDisease ProgressionHumansLiverTransforming Growth Factor beta1Transforming Growth Factor beta1anti-oxidant systemECMfibrosisinflammationorgan malfunctionTGF-β

Identifiers

PMID36835428
PMCPMC9963026
OpenAlexW4321242142

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.