Evidence map›Paper›PMID 17333393›Full record

ReviewPharmaceutical research2007

New insights into the pathogenesis and treatment of idiopathic pulmonary fibrosis: a potential role for stem cells in the lung parenchyma and implications for therapy.

Mehrnaz Gharaee-Kermani, Margaret R Gyetko, Biao Hu, Sem H Phan

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pharmaceutical research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
8.5field-weighted citation impact, top 2% 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

49 citing papers in PubMed, 106 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Update on Novel Targeted Therapy for Pleural Organization and Fibrosis.International journal of molecular sciences · 2022
    Review
  7. Pharmaceutics · 2021
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Reduced FoxO3a expression causes low autophagy in idiopathic pulmonary fibrosis fibroblasts on collagen matrices.American journal of physiology. Lung cellular and molecular physiology · 2015
    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

4 authors at 1 institution in 1 country.

Mehrnaz Gharaee-KermaniDivision of Pulmonary Medicine & Critical Care, Department of Internal Medicine, University of Michigan Medical School, 2215 Fuller Rd. VAMC 11R, Ann Arbor, Michigan 48105, USA. nazy@umich.edu
Margaret R Gyetko
Biao Hu
Sem H Phan
University of Michigan–Ann Arbor · US

Funding

MONONUCLEAR LEUKOCYTE ADHESION AND RECRUITMENT IN CHRONIC INFLAMMATORY DISEASEP01HL031963 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LUKACS, NICHOLAS W · 1985 to 2009
$14.1M
MYOFIBROBLASTS IN PULMONARY FIBROSISR01HL052285 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PHAN, SEM H · 1994 to 2017
$5.4M
Mechanisms of Pulmonary FibrosisR37HL028737 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PHAN, SEM H · 2001 to 2010
$3.0M
Novel telomerase expressing lung fibroblast phenotypeR01HL077297 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PHAN, SEM H · 2004 to 2012
$3.0M
MECHANISMS OF PULMONARY FIBROSISR01HL028737 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PHAN, SEM H · 1986 to 2000
$227k
NHLBI NIH HHS HL28737NHLBI NIH HHS HL31963NHLBI NIH HHS HL52285NHLBI NIH HHS HL77297
6 · The paper itself

Abstract

Idiopathic Pulmonary Fibrosis (IPF) is a chronic, progressive, and often fatal form of interstitial lung disease. It is characterized by injury with loss of lung epithelial cells and abnormal tissue repair, resulting in replacement of normal functional tissue, abnormal accumulation of fibroblasts and myofibroblasts, deposition of extracellular matrix, and distortion of lung architecture which results in respiratory failure. Despite improvements in the diagnostic approach to IPF and active research in recent years, the molecular mechanisms of the disease remain poorly understood. This highly lethal lung disorder continues to pose major clinical challenges since an effective therapeutic regimen has yet to be identified and developed. For example, a treatment modality has been based on the assumption that IPF is a chronic inflammatory disease, yet most available anti-inflammatory drugs are not effective in treating it. Hence researchers are now focusing on understanding alternative underlying mechanisms involved in the pathogenesis of IPF in the hope of discovering potentially new pharmaceutical targets. This paper will focus on lung tissue repair, regeneration, remodeling, and cell types that may be important to consider in therapeutic interventions and includes a more detailed discussion of the potential targets of current therapeutic attack in pulmonary fibrosis. The discovery that adult bone marrow stem cells can contribute to the formation of differentiated cell types in other tissues, especially after injury, implies that they have the potential to participate in tissue remodeling, and perhaps regeneration. The current promise of the use of adult stem cells for tissue regeneration, and the belief that once irreversibly damaged tissue could be restored to a normal functional capacity using stem cell-based therapy, suggests a novel approach for treatment of diverse chronic diseases. However this optimism is tempered by current evidence that the pathogenesis of pulmonary fibrosis may involve the recruitment of bone marrow-derived fibroblasts, which are the key contributors to the pathogenesis of this chronic progressive disorder. Nevertheless, stem cell-related therapies are widely viewed as promising treatment options for patients suffering from various types of pulmonary diseases. Gender mismatched bone marrow or lung transplant recipients serve as natural populations in which to study the role of bone marrow-derived stem cells in recovery from pulmonary diseases. Understanding the mechanism of recruitment of stem cells to sites of injury, and their involvement in tissue repair, regeneration, and remodeling may offer a novel therapeutic target for developing more effective treatments against this fatal disorder. This article reviews the new concepts in the pathogenesis, current and future treatment options of pulmonary fibrosis, and the recent advances regarding the roles of stem cells in lung tissue repair, regeneration, and remodeling.

Indexed as

Adult Stem CellsAnimalsHumansLungModels, BiologicalPulmonary FibrosisRegenerationTargeted Gene Repair

Identifiers

PMID17333393
OpenAlexW2075408403

What OpenQuestion holds

Textmetadata
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.