Evidence map›Paper›PMID 38375579›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2024

Anti-inflammatory roles of type I interferon signaling in the lung.

Jingjing Feng, Yi Liu, Jooyoung Kim, Farida Ahangari, Naftali Kaminski, William G Bain, Zhijun Jie, Charles S Dela Cruz, Lokesh Sharma

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

7 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Interstitial lung disease and the STING pathway.The Journal of clinical investigation · 2026
    Review
  3. Article
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  6. Genome-wide screen inbioRxiv : the preprint server for biology · 2025
    Article
  7. 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

9 authors at 3 institutions in 2 countries.

Jingjing FengDepartment of Pulmonary and Critical Care Medicine, Shanghai Fifth People's Hospital, Center of Community-Based Health Research, Fudan University, Shanghai, China.
Yi LiuShanghai Emerging and Re-emerging Institute, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Jooyoung KimDivision of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States.
Farida AhangariSection of Pulmonary, Critical Care and Sleep Medicine, Yale School of Medicine, New Haven, Connecticut, United States.
Naftali KaminskiSection of Pulmonary, Critical Care and Sleep Medicine, Yale School of Medicine, New Haven, Connecticut, United States.ORCID 0000-0001-5917-4601
William G BainDivision of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States.ORCID 0000-0001-8506-0552
Zhijun JieDepartment of Pulmonary and Critical Care Medicine, Shanghai Fifth People's Hospital, Center of Community-Based Health Research, Fudan University, Shanghai, China.
Charles S Dela CruzSection of Pulmonary, Critical Care and Sleep Medicine, Yale School of Medicine, New Haven, Connecticut, United States.
Lokesh SharmaSection of Pulmonary, Critical Care and Sleep Medicine, Yale School of Medicine, New Haven, Connecticut, United States.ORCID 0000-0003-3040-9029
University of Pittsburgh · USFudan University · CNYale University · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
American Lung Association (ALA) CatalystBLRD VA I01 BX004661Francis Family Foundation (FF)NCATS NIH HHS UL1 TR001863| Shanghai Minhang Health And Family Planning Commission () 2020MZYS12Shanghai Minhang Science and Technology Commission () 2022MHZ005U.S. Department of Defense (DOD)U.S. Department of Veterans Affairs (VA) BX004661
6 · The paper itself

Abstract

Excessive or persistent inflammation may have detrimental effects on lung structure and function. Currently, our understanding of conserved host mechanisms that control the inflammatory response remains incompletely understood. In this study, we investigated the role of type I interferon signaling in the inflammatory response against diverse clinically relevant stimuli. Using mice deficient in type I interferon signaling (IFNAR1

Indexed as

Interferon Type ILungMice, Inbred C57BLMice, KnockoutReceptor, Interferon alpha-betaSignal TransductionAnimalsBleomycinInflammationLipopolysaccharidesMaleMicePseudomonas aeruginosaPseudomonas InfectionsBleomycinIfnar1 protein, mouseInterferon Type ILipopolysaccharidesReceptor, Interferon alpha-betableomycininterferonLPSlung inflammationPseudomonas

Identifiers

PMID38375579
PMCPMC11380987
OpenAlexW4391970524

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.