Evidence map›Paper›PMID 25090037›Full record

ReviewAmerican journal of respiratory and critical care medicine2014

New therapeutic targets in idiopathic pulmonary fibrosis. Aiming to rein in runaway wound-healing responses.

Neil Ahluwalia, Barry S Shea, Andrew M Tager

Abstract readReview
In one paragraph

Review in American journal of respiratory and critical care medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed, 1 pooled it
20.3field-weighted citation impact, top 1% 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

124 citing papers in PubMed, 1 synthesis or guideline pooled it, 230 citations in OpenAlex.

  1. Pooled it
  2. LPARespiratory research · 2022
    Trial
  3. Trial
  4. PulmonaryEuropean journal of nuclear medicine and molecular imaging · 2018
    Trial
  5. Trial
  6. Article
  7. Protective Role of Octreotide in Acute and Chronic Lung Injuries.International journal of preventive medicine · 2026
    Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Circulating biomarker analyses in a longitudinal cohort of patients with IPF.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  17. Review
  18. Review
  19. DNA methylation modification in Idiopathic pulmonary fibrosis.Frontiers in cell and developmental biology · 2024
    Review
  20. Article

64 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 1 institution in 1 country.

Neil AhluwaliaPulmonary and Critical Care Unit and Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.
Barry S Shea
Andrew M Tager
Harvard University · US

Funding

Research Training in Pulmonary Immunology and Allergy at MGHT32HL116275 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI David C Christiani, ANDREW D LUSTER · 2013 to 2026
$8.6M
Protective Role of the S1P-S1P1 Pathway in Pulmonary FibrosisR01HL108975 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI TAGER, ANDREW M · 2011 to 2015
$1.8M
The LPA Pathway in Lung Fibrosis: Novel Mediators and New Therapeutic TargetsR01HL095732 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI TAGER, ANDREW M · 2009 to 2010
$922k
The Role of Sphingosine 1-Phosphate in Lung Injury and FibrosisK08HL105656 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI SHEA, BARRY S. · 2011 to 2015
$683k
NHLBI NIH HHS K08 HL105656NHLBI NIH HHS K08HL105656NHLBI NIH HHS R01 HL095732NHLBI NIH HHS R01HL095732NHLBI NIH HHS R01 HL108975NHLBI NIH HHS R01HL108975NHLBI NIH HHS T32 HL116275NHLBI NIH HHS T32HL116275
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a devastating disease, with a median survival as short as 3 years from the time of diagnosis and no pharmacological therapies yet approved by the U.S. Food and Drug Administration. To address the great unmet need for effective IPF therapy, a number of new drugs have recently been, or are now being, evaluated in clinical trials. The rationales for most of these therapeutic candidates are based on the current paradigm of IPF pathogenesis, in which recurrent injury to the alveolar epithelium is believed to drive aberrant wound healing responses, resulting in fibrosis rather than repair. Here we discuss drugs in recently completed or currently ongoing phase II and III IPF clinical trials in the context of their putative mechanisms of action and the aberrant repair processes they are believed to target: innate immune activation and polarization, fibroblast accumulation and myofibroblast differentiation, or extracellular matrix deposition and stiffening. Placed in this context, the positive results of recently completed trials of pirfenidone and nintedanib, and results that will come from ongoing trials of other agents, should provide valuable insights into the still-enigmatic pathogenesis of this disease, in addition to providing benefits to patients with IPF.

Indexed as

Anti-Inflammatory Agents, Non-SteroidalAntioxidantsClinical Trials, Phase II as TopicClinical Trials, Phase III as TopicEnzyme InhibitorsHumansIdiopathic Pulmonary FibrosisImmunosuppressive AgentsIndolesPyridonesWound HealingAnti-Inflammatory Agents, Non-SteroidalAntioxidantsEnzyme InhibitorsImmunosuppressive AgentsIndolesnintedanibpirfenidonePyridonesidiopathic pulmonary fibrosisinvestigational treatmentspathogenesis

Identifiers

PMID25090037
PMCPMC4299574
OpenAlexW2045730105

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.