Evidence map›Paper›PMID 28417017›Full record

ArticleCell death discovery2017

Galectin-1 inhibition attenuates profibrotic signaling in hypoxia-induced pulmonary fibrosis.

Jaymin J Kathiriya, Niyati Nakra, Jenna Nixon, Puja S Patel, Vijay Vaghasiya, Ahmed Alhassani, Zhi Tian, Diane Allen-Gipson, Vrushank Davé

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

34 citing papers in PubMed, 46 citations in OpenAlex.

  1. Trial
  2. Targeting the CD4Molecular biomedicine · 2026
    Article
  3. Review
  4. Article
  5. Review
  6. Targeting Fibrosis: From Molecular Mechanisms to Advanced Therapies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Regulation of wound healing and fibrosis by galectins.Journal of molecular medicine (Berlin, Germany) · 2022
    Review
  19. Article
  20. Galectin 1-A Key Player between Tissue Repair and Fibrosis.International journal of molecular sciences · 2022
    Review
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

9 authors at 2 institutions in 1 country.

Jaymin J KathiriyaDepartment of Pathology and Cell Biology, Morsani College of Medicine, University of South Florida, Tampa, FL 33612, USA.
Niyati NakraDepartment of Pathology and Cell Biology, Morsani College of Medicine, University of South Florida, Tampa, FL 33612, USA.
Jenna NixonDepartment of Pathology and Cell Biology, Morsani College of Medicine, University of South Florida, Tampa, FL 33612, USA.
Puja S PatelUniversity of Miami, Coral Gables, FL 33124, USA.
Vijay VaghasiyaDepartment of Pathology and Cell Biology, Morsani College of Medicine, University of South Florida, Tampa, FL 33612, USA.
Ahmed AlhassaniDepartment of Pathology and Cell Biology, Morsani College of Medicine, University of South Florida, Tampa, FL 33612, USA.
Zhi TianUniversity of Miami, Coral Gables, FL 33124, USA.
Diane Allen-GipsonDepartment of Pharmaceutical Science, College of Pharmacy, University of South Florida, Tampa, FL 33612, USA.
Vrushank DavéDepartment of Pathology and Cell Biology, Morsani College of Medicine, University of South Florida, Tampa, FL 33612, USA.
University of South Florida · USUniversity of Miami · US

Funding

Hypoxia Signaling and Spontaneous Pulmonary Fibrosis in a Novel Mouse ModelR21AG047473 · NIA · UNIVERSITY OF SOUTH FLORIDA · PI DAVE, VRUSHANK · 2015 to 2016
$426k
NIA NIH HHS R21 AG047473
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is characterized by lung remodeling arising from epithelial injury, aberrant fibroblast growth, and excessive deposition of extracellular matrix. Repeated epithelial injury elicits abnormal wound repair and lung remodeling, often associated with alveolar collapse and edema, leading to focal hypoxia. Here, we demonstrate that hypoxia is a physiological insult that contributes to pulmonary fibrosis (PF) and define its molecular roles in profibrotic activation of lung epithelial cells. Hypoxia increased transcription of profibrotic genes and altered the proteomic signatures of lung epithelial cells. Network analysis of the hypoxic epithelial proteome revealed a crosstalk between transforming growth factor-

Identifiers

PMID28417017
PMCPMC5385413
OpenAlexW2607334934

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.