Evidence map›Paper›PMID 30985294›Full record

ArticleThe Journal of clinical investigation2019

Yap/Taz regulate alveolar regeneration and resolution of lung inflammation.

Ryan LaCanna, Daniela Liccardo, Peggy Zhang, Lauren Tragesser, Yan Wang, Tongtong Cao, Harold A Chapman, Edward E Morrisey, Hao Shen, Walter J Koch and 3 more

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07488988 (SCARFREE-001), which is not on this map. Cited by 185 papers.

0numbers the graph read from it
0cells of the map it votes in
185citing papers in PubMed
14.3field-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.

NCT07488988 phase2not yet recruitingnot on this mapstarted 2026, after this paper: background citation

SCARFREE-001: A Phase 2 Dose-Finding and Proof-of-Concept Study of Intradermal Verteporfin for Scar Prevention in Open and Closed Surgical Wounds

TypeinterventionalSponsorOdense University HospitalRan2026 to 2028Enrolled12ConditionsSurgical ScarArmsVerteporfin Injection, Saline injection
3 · Its place in the literature

Who cites it

185 citing papers in PubMed, 299 citations in OpenAlex.

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  19. Airway Goblet Metaplasia Resulting from YAP/TAZ Deletion Drives Pulmonary Inflammatory Responses.American journal of respiratory cell and molecular biology · 2026
    Article
  20. Review

125 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

13 authors at 3 institutions in 1 country.

Ryan LaCannaDepartment of Pharmacology, Center for Translational Medicine, Temple University Lewis Katz School of Medicine, Philadelphia, Pennsylvania, USA.
Daniela LiccardoDepartment of Pharmacology, Center for Translational Medicine, Temple University Lewis Katz School of Medicine, Philadelphia, Pennsylvania, USA.
Peggy ZhangDepartment of Pharmacology, Center for Translational Medicine, Temple University Lewis Katz School of Medicine, Philadelphia, Pennsylvania, USA.
Lauren TragesserDepartment of Pharmacology, Center for Translational Medicine, Temple University Lewis Katz School of Medicine, Philadelphia, Pennsylvania, USA.
Yan WangDepartment of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Tongtong CaoDepartment of Pharmacology, Center for Translational Medicine, Temple University Lewis Katz School of Medicine, Philadelphia, Pennsylvania, USA.
Harold A ChapmanDepartment of Medicine, Cardiovascular Research Institute, UCSF, San Francisco, California, USA.
Edward E MorriseyDepartment of Medicine, Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Hao ShenDepartment of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Walter J KochDepartment of Pharmacology, Center for Translational Medicine, Temple University Lewis Katz School of Medicine, Philadelphia, Pennsylvania, USA.
Beata KosmiderDepartment of Physiology, Department of Thoracic Medicine and Surgery, Center for Inflammation, Translational and Clinical Lung Research, Temple University Lewis Katz School of Medicine, Philadelphia, Pennsylvania, USA.
Marla R WolfsonDepartment of Physiology, Department of Thoracic Medicine and Surgery, Center for Inflammation, Translational and Clinical Lung Research, Temple University Lewis Katz School of Medicine, Philadelphia, Pennsylvania, USA.
Ying TianDepartment of Pharmacology, Center for Translational Medicine, Temple University Lewis Katz School of Medicine, Philadelphia, Pennsylvania, USA.
Temple University · USUniversity of Pennsylvania · USUniversity of California, San Francisco · US

Funding

Regulation of distal lung epithelial regeneration by microRNA-Hippo pathwayR01HL132115 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI TIAN, YING · 2016 to 2020
$2.0M
DJ-1 pathway impairment in alveolar type II cells in emphysema.R01HL118171 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI KOSMIDER, BEATA · 2014 to 2018
$2.0M
miRNAs regulate lung epithelial progenitor cells in development and injury repairR00HL111348 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI TIAN, YING · 2014 to 2016
$747k
NHLBI NIH HHS R00 HL111348NHLBI NIH HHS R01 HL118171NHLBI NIH HHS R01 HL132115
6 · The paper itself

Abstract

Alveolar epithelium plays a pivotal role in protecting the lungs from inhaled infectious agents. Therefore, the regenerative capacity of the alveolar epithelium is critical for recovery from these insults in order to rebuild the epithelial barrier and restore pulmonary functions. Here, we show that sublethal infection of mice with Streptococcus pneumoniae, the most common pathogen of community-acquired pneumonia, led to exclusive damage in lung alveoli, followed by alveolar epithelial regeneration and resolution of lung inflammation. We show that surfactant protein C-expressing (SPC-expressing) alveolar epithelial type II cells (AECIIs) underwent proliferation and differentiation after infection, which contributed to the newly formed alveolar epithelium. This increase in AECII activities was correlated with increased nuclear expression of Yap and Taz, the mediators of the Hippo pathway. Mice that lacked Yap/Taz in AECIIs exhibited prolonged inflammatory responses in the lung and were delayed in alveolar epithelial regeneration during bacterial pneumonia. This impaired alveolar epithelial regeneration was paralleled by a failure to upregulate IκBa, the molecule that terminates NF-κB-mediated inflammatory responses. These results demonstrate that signals governing resolution of lung inflammation were altered in Yap/Taz mutant mice, which prevented the development of a proper regenerative niche, delaying repair and regeneration of alveolar epithelium during bacterial pneumonia.

Indexed as

Adaptor Proteins, Signal TransducingAlveolar Epithelial CellsAnimalsCell Cycle ProteinsCell DifferentiationCell NucleusCell ProliferationEpithelial CellsEpitheliumHEK293 CellsHumansInflammationLungMaleMiceMice, Inbred C57BLAdaptor Proteins, Signal TransducingCell Cycle ProteinsNF-kappa BPulmonary Surfactant-Associated Protein CSftpc protein, mouseTrans-ActivatorsWwtr1 protein, mouseYap1 protein, mouseYAP-Signaling ProteinsAdult stem cellsBacterial infectionsPulmonologyStem cells

Identifiers

PMID30985294
PMCPMC6486331
OpenAlexW2938109071

What OpenQuestion holds

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Registered trials

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.