Evidence map›Paper›PMID 34258628›Full record

ReviewJournal of molecular medicine (Berlin, Germany)2021

The interplay of DAMPs, TLR4, and proinflammatory cytokines in pulmonary fibrosis.

Siavash Bolourani, Max Brenner, Ping Wang

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of molecular medicine (Berlin, Germany), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
9.7field-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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Roles of the Altitude-Adapted Immune Microenvironment in Pulmonary Vascular Remodeling in High-Altitude Pulmonary Hypertension: A Review.Medical science monitor : international medical journal of experimental and clinical research · 2026
    Review
  11. Article
  12. Article
  13. Immune dysregulation inFrontiers in immunology · 2026
    Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. eNAMPT Is a Novel DAMP and Therapeutic Target in Human and Murine Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2025
    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

3 authors at 2 institutions in 1 country.

Siavash BolouraniCenter for Immunology and Inflammation, Feinstein Institutes for Medical Research, 350 Community Dr, Manhasset, NY, 11030, USA.
Max BrennerCenter for Immunology and Inflammation, Feinstein Institutes for Medical Research, 350 Community Dr, Manhasset, NY, 11030, USA. mbrenner@northwell.edu.ORCID 0000-0002-8010-148X
Ping WangCenter for Immunology and Inflammation, Feinstein Institutes for Medical Research, 350 Community Dr, Manhasset, NY, 11030, USA. pwang@northwell.edu.ORCID 0000-0002-1557-0394
Northwell Health · USFeinstein Institute for Medical Research · US

Funding

IMPROVEMENT OF ORGAN FUNCTION AFTER SEVERE HYPOVOLEMIAR01HL076179 · NHLBI · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI PING WANG · 2004 to 2026
$7.6M
Novel Approaches to Maintaining Organ Function in SepsisR35GM118337 · NIGMS · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI PING WANG · 2016 to 2026
$5.2M
NHLBI NIH HHS R01 HL076179NHLBI NIH HHS R01HL076179NIGMS NIH HHS R35 GM118337NIGMS NIH HHS R35GM118337
6 · The paper itself

Abstract

Pulmonary fibrosis is a chronic debilitating condition characterized by progressive deposition of connective tissue, leading to a steady restriction of lung elasticity, a decline in lung function, and a median survival of 4.5 years. The leading causes of pulmonary fibrosis are inhalation of foreign particles (such as silicosis and pneumoconiosis), infections (such as post COVID-19), autoimmune diseases (such as systemic autoimmune diseases of the connective tissue), and idiopathic pulmonary fibrosis. The therapeutics currently available for pulmonary fibrosis only modestly slow the progression of the disease. This review is centered on the interplay of damage-associated molecular pattern (DAMP) molecules, Toll-like receptor 4 (TLR4), and inflammatory cytokines (such as TNF-α, IL-1β, and IL-17) as they contribute to the pathogenesis of pulmonary fibrosis, and the possible avenues to develop effective therapeutics that disrupt this interplay.

Indexed as

AlarminsAnimalsCytokinesHumansIdiopathic Pulmonary FibrosisInflammationModels, BiologicalToll-Like Receptor 4AlarminsCytokinesToll-Like Receptor 4CytokineDAMPPulmonary fibrosisTLR4

Identifiers

PMID34258628
PMCPMC8277227
OpenAlexW3178172899

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.