Evidence map›Paper›PMID 28035951›Full record

ReviewJournal of clinical medicine2016

A Systematic Review of the Role of Dysfunctional Wound Healing in the Pathogenesis and Treatment of Idiopathic Pulmonary Fibrosis.

Alan Betensley, Rabab Sharif, Dimitrios Karamichos

Open access · goldAbstract readReview
In one paragraph

Review in Journal of clinical medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

71 citing papers in PubMed, 117 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. S100A4 Orchestrates Fibroblast Fate to Drive Fibrotic Remodeling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. The intersection of liver cirrhosis and pulmonary fibrosis.Journal of translational medicine · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. MitochondrialInternational journal of molecular sciences · 2025
    Article
  15. Article
  16. Article
  17. Leukemia inhibitory factor (LIF) receptor amplifies pathogenic activation of fibroblasts in lung fibrosis.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  18. Article
  19. Review
  20. Article

11 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

3 authors at 3 institutions in 1 country.

Alan BetensleyNazih Zuhdi Transplant Institute, Integris Baptist Medical Center, Oklahoma City, OK 73112, USA. alan.betensley@integrisok.com.
Rabab SharifDepartment of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA. rabab-sharif@ouhsc.edu.
Dimitrios KaramichosDepartment of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA. dimitrios-karamichos@ouhsc.edu.
Dean McGee Eye Institute · USINTEGRIS Baptist Medical Center · USUniversity of Oklahoma Health Sciences Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive interstitial lung disorder showcasing an interaction between genetic predisposition and environmental risks. This usually involves the coaction of a mixture of cell types associated with abnormal wound healing, leading to structural distortion and loss of gas exchange function. IPF bears fatal prognosis due to respiratory failure, revealing a median survival of approximately 2 to 3 years. This review showcases the ongoing progress in understanding the complex pathophysiology of IPF and it highlights the latest potential clinical treatments. In IPF, various components of the immune system, particularly clotting cascade and shortened telomeres, are highly involved in disease pathobiology and progression. This review also illustrates two US Food and Drug Administration (FDA)-approved drugs, nintedanib (OFEV, Boehringer Ingelheim, Ingelheim am Rhein, Germany) and pirfenidone (Esbriet, Roche, Basel, Switzerland), that slow IPF progression, but unfortunately neither drug can reverse the course of the disease. Although the mechanisms underlying IPF remain poorly understood, this review unveils the past and current advances that encourage the detection of new IPF pathogenic pathways and the development of effective treatment methods for the near future.

Indexed as

chronic lung allograft dysfunctionextracellular matrix remodelingidiopathic pulmonary fibrosislung transplantation

Identifiers

PMID28035951
PMCPMC5294955
OpenAlexW2567257918

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.