Evidence map›Paper›PMID 18264692›Full record

ReviewIntensive care medicine2008

Advances in mechanisms of repair and remodelling in acute lung injury.

Claudia C Dos Santos

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Intensive care medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 2 pooled it
6.6field-weighted citation impact, top 3% 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

36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 94 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. PTPα promotes fibroproliferative responses after acute lung injury.American journal of physiology. Lung cellular and molecular physiology · 2022
    Article
  10. From ARDS to pulmonary fibrosis: the next phase of the COVID-19 pandemic?Translational research : the journal of laboratory and clinical medicine · 2022
    Review
  11. Molecular mechanisms of postintensive care syndrome.Intensive care medicine experimental · 2021
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Plasma membrane wounding and repair in pulmonary diseases.American journal of physiology. Lung cellular and molecular physiology · 2017
    Review
  18. Article
  19. Article
  20. Enhanced resolution of experimental ARDS through IL-4-mediated lung macrophage reprogramming.American journal of physiology. Lung cellular and molecular physiology · 2016
    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

1 author at 1 institution in 1 country.

Claudia C Dos SantosInterdepartmental Division of Critical Care, University of Toronto, 30, Bond Street 4-008, M5G 1W8, Toronto, Ontario, Canada. Claudia.santos@utoronto.ca
University of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcute respiratory distress syndrome (ARDS) is the most severe manifestation of acute lung injury (ALI). In patients who survive the acute injury the process of repair and remodelling may be an independent risk factor determining morbidity and mortality. This review explores recent advances in the field of fibroproliferative ARDS/ALI, with a special emphasis on (a) the primary contributing factors with a focus on cellular and soluble factors, and (b) mechanisms involved in repair and remodelling as they pertain to the importance of cell death, re-population, and matrix deposition. DISCUSSION: Factors influencing progression to fibroproliferative ARDS vs. resolution and reconstitution of the normal pulmonary parenchymal architecture are poorly understood. Determinants of persistent injury and abnormal repair and remodelling may be profoundly affected by both environmental and genetic factors. Moreover, cumulative evidence suggests that acute inflammation and fibrosis may be in part independent and interactive processes that are autonomously regulated and thus amenable to individual and specific therapy.

conclusionsAlthough our current understanding of these processes is limited by the inability to accurately replicate the complex human physiology in laboratory settings, it has recently become apparent that the process of repair and remodelling begins early in the course of ARDS/ALI and may be determined by the type of pulmonary injury. Understanding the mechanisms leading to and regulating fibroproliferative changes may contribute to the development of novel early therapeutic interventions in ARDS/ALI patients.

Indexed as

Extracellular MatrixHumansModels, BiologicalPulmonary AlveoliPulmonary FibrosisRegenerationRespiratory Distress SyndromeRespiratory Mucosa

Identifiers

PMID18264692
OpenAlexW2102111220

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.