Evidence map›Paper›PMID 31434287›Full record

ArticleCells2019

DROSHA-Dependent AIM2 Inflammasome Activation Contributes to Lung Inflammation during Idiopathic Pulmonary Fibrosis.

Soo Jung Cho, Kyoung Sook Hong, Ji Hun Jeong, Mihye Lee, Augustine M K Choi, Heather W Stout-Delgado, Jong-Seok Moon

Open access · goldAbstract read
In one paragraph

Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 39 citations in OpenAlex.

  1. Inflammasomes in respiratory diseases: from disease pathogenesis to drug development and use of multi-omics.European respiratory review : an official journal of the European Respiratory Society · 2026
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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

7 authors at 2 institutions in 2 countries.

Soo Jung ChoJoan and Sanford I. Weill Department of Medicine, Weill Cornell Medical College, New York-Presbyterian Hospital, New York, NY 10011, USA.
Kyoung Sook HongJoan and Sanford I. Weill Department of Medicine, Weill Cornell Medical College, New York-Presbyterian Hospital, New York, NY 10011, USA.
Ji Hun JeongDepartment of Integrated Biomedical Science, Soonchunhyang Institute of Medi-bio Science (SIMS), Soonchunhyang University, Cheonan-si 31151, Korea.
Mihye LeeDepartment of Integrated Biomedical Science, Soonchunhyang Institute of Medi-bio Science (SIMS), Soonchunhyang University, Cheonan-si 31151, Korea.
Augustine M K ChoiJoan and Sanford I. Weill Department of Medicine, Weill Cornell Medical College, New York-Presbyterian Hospital, New York, NY 10011, USA.
Heather W Stout-DelgadoJoan and Sanford I. Weill Department of Medicine, Weill Cornell Medical College, New York-Presbyterian Hospital, New York, NY 10011, USA.
Jong-Seok MoonDepartment of Integrated Biomedical Science, Soonchunhyang Institute of Medi-bio Science (SIMS), Soonchunhyang University, Cheonan-si 31151, Korea. jongseok81@sch.ac.kr.ORCID 0000-0002-2537-7854
NewYork–Presbyterian Hospital · USSoonchunhyang University · KR

Funding

Respiratory Computational Discovery CoreP01HL114501 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI SILVERMAN, EDWIN K · 2013 to 2025
$24.9M
Impact of Heightened UPR Activation on Inflammasome Responses to Influenza and Secondary Streptococcus pneumoniae Infection in Aged LungR01AG056699 · NIA · WEILL MEDICAL COLL OF CORNELL UNIV · PI STOUT DELGADO, HEATHER WINONA · 2018 to 2022
$2.6M
Impact of Heightened ER Stress on NLRP3 Activation in Aged Lung during InfectionR01AG052530 · NIA · WEILL MEDICAL COLL OF CORNELL UNIV · PI STOUT DELGADO, HEATHER WINONA · 2017 to 2021
$2.1M
GLUT1-dependent glycolysis regulates age-susceptible lung fibrosisK08HL138285 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CHO, SOO JUNG · 2017 to 2021
$829k
NHLBI NIH HHS K08 HL138285NHLBI NIH HHS P01 HL114501NIA NIH HHS R01 AG052530NIA NIH HHS R01 AG056699
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) has been linked to chronic lung inflammation. Drosha ribonuclease III (DROSHA), a class 2 ribonuclease III enzyme, plays a key role in microRNA (miRNA) biogenesis. However, the mechanisms by which DROSHA affects the lung inflammation during idiopathic pulmonary fibrosis (IPF) remain unclear. Here, we demonstrate that DROSHA regulates the absent in melanoma 2 (AIM2) inflammasome activation during idiopathic pulmonary fibrosis (IPF). Both DROSHA and AIM2 protein expression were elevated in alveolar macrophages of patients with IPF. We also found that DROSHA and AIM2 protein expression were increased in alveolar macrophages of lung tissues in a mouse model of bleomycin-induced pulmonary fibrosis. DROSHA deficiency suppressed AIM2 inflammasome-dependent caspase-1 activation and interleukin (IL)-1β and IL-18 secretion in primary mouse alveolar macrophages and bone marrow-derived macrophages (BMDMs). Transduction of microRNA (miRNA) increased the formation of the adaptor apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) specks, which is required for AIM2 inflammasome activation in BMDMs. Our results suggest that DROSHA promotes AIM2 inflammasome activation-dependent lung inflammation during IPF.

Indexed as

PneumoniaAdultAgedAnimalsCells, CulturedChronic DiseaseDNA-Binding ProteinsFemaleHumansIdiopathic Pulmonary FibrosisInflammasomesMacrophagesMacrophages, AlveolarMaleMiceMice, Inbred C57BLAIM2 protein, humanDNA-Binding ProteinsDROSHA protein, humanInflammasomesRibonuclease IIIAIM2 inflammasomeDROSHAidiopathic pulmonary fibrosismiRNA

Identifiers

PMID31434287
PMCPMC6721825
OpenAlexW2969915502

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.