Evidence map›Paper›PMID 31011925›Full record

ReviewInflammation2019

Acute Lung Injury: IL-17A-Mediated Inflammatory Pathway and Its Regulation by Curcumin.

Mahesh Manjunath Gouda, Yashodhar Prabhakar Bhandary

Abstract readReview
PubMed Publisher
In one paragraph

Review in Inflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 4% 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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.

  1. Pooled it
  2. Review
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  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Anti-Inflammatory Activity of BiotransformedJournal of microbiology and biotechnology · 2024
    Article
  12. Review
  13. Pulmonary toxicity of immune checkpoint immunotherapy.The Journal of clinical investigation · 2024
    Review
  14. Article
  15. Article
  16. Review
  17. Interleukins: pathophysiological role in acute pancreatitis.Archives of medical science : AMS · 2024
    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

2 authors at 1 institution in 1 country.

Mahesh Manjunath GoudaYenepoya Research Centre, Yenepoya University, Deralakatte, Mangalore, Karnataka, 575018, India.
Yashodhar Prabhakar BhandaryYenepoya Research Centre, Yenepoya University, Deralakatte, Mangalore, Karnataka, 575018, India. yash28bhandary@gmail.com.
Yenepoya University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute lung injury (ALI) is characterized by acute inflammation and tissue injury results in dysfunction of the alveolar epithelial membrane. If the epithelial injury is severe, a fibroproliferative phase of ALI can develop. During this phase, the activated fibroblast and myofibroblasts synthesize excessive collagenous extracellular matrix that leads to a condition called pulmonary fibrosis. Lung injury can be caused by several ways; however, the present review focus on bleomycin (BLM)-mediated changes in the pathology of lungs. BLM is a chemotherapeutic agent and has toxic effects on lungs, which leads to oxidative damage and elaboration of inflammatory cytokines. In response to the injury, the inflammatory cytokines will be activated to defend the system from injury. These cytokines along with growth factors stimulate the proliferation of myofibroblasts and secretion of pathologic extracellular matrix. During BLM injury, the pro-inflammatory cytokine such as IL-17A will be up-regulated and mediates the inflammation in the alveolar epithelial cell and also brings about recruitment of certain inflammatory cells in the alveolar surface. These cytokines probably help in up-regulating the expression of p53 and fibrinolytic system molecules during the alveolar epithelial cells apoptosis. Here, our key concern is to provide the adequate knowledge about IL-17A-mediated p53 fibrinolytic system and their pathogenic progression to pulmonary fibrosis. The present review focuses mainly on IL-17A-mediated p53-fibrinolytic aspects and how curcumin is involved in the regulation of pathogenic progression of ALI and pulmonary fibrosis.

Indexed as

Acute Lung InjuryAlveolar Epithelial CellsAnimalsBleomycinCurcuminHumansInflammationInterleukin-17Pulmonary FibrosisTumor Suppressor Protein p53BleomycinCurcuminIL17A protein, humanInterleukin-17Tumor Suppressor Protein p53Acute lung injury (ALI)Bleomycin (BLM)curcuminInterleukin-17A (IL-17A)p53plasminogen activator inhibitor-I (PAI-I)Pulmonary fibrosis (PF)urokinase plasminogen activator receptor (uPAR)urokinase plasminogen activator (uPA)

Identifiers

PMID31011925
OpenAlexW2940519842

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.