Evidence map›Paper›PMID 32398133›Full record

ReviewRespiratory research2020

Cathepsin S: investigating an old player in lung disease pathogenesis, comorbidities, and potential therapeutics.

Ryan Brown, Sridesh Nath, Alnardo Lora, Ghassan Samaha, Ziyad Elgamal, Ryan Kaiser, Clifford Taggart, Sinéad Weldon, Patrick Geraghty

Open access · goldAbstract readReview
In one paragraph

Review in Respiratory research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.1field-weighted citation impact, top 4% 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

55 citing papers in PubMed, 86 citations in OpenAlex.

  1. Trial
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  15. Origin and stepwise evolution of vertebrate lungs.Nature ecology & evolution · 2025
    Article
  16. Dipeptidyl peptidase-1 inhibitors in bronchiectasis.European respiratory review : an official journal of the European Respiratory Society · 2025
    Review
  17. Article
  18. Review
  19. Article
  20. Advances in Cathepsin S Inhibition: Challenges and Breakthroughs in Drug Development.Pathophysiology : the official journal of the International Society for Pathophysiology · 2024
    Review
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 2 institutions in 2 countries.

Ryan BrownAirway Innate Immunity Research (AiiR) Group, Wellcome-Wolfson Institute for Experimental Medicine, School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast, Belfast, Northern Ireland, UK.
Sridesh NathDivision of Pulmonary & Critical Care Medicine, Department of Medicine, State University of New York Downstate Medical Centre, Brooklyn, NY, USA.
Alnardo LoraDivision of Pulmonary & Critical Care Medicine, Department of Medicine, State University of New York Downstate Medical Centre, Brooklyn, NY, USA.
Ghassan SamahaDivision of Pulmonary & Critical Care Medicine, Department of Medicine, State University of New York Downstate Medical Centre, Brooklyn, NY, USA.
Ziyad ElgamalDivision of Pulmonary & Critical Care Medicine, Department of Medicine, State University of New York Downstate Medical Centre, Brooklyn, NY, USA.
Ryan KaiserDivision of Pulmonary & Critical Care Medicine, Department of Medicine, State University of New York Downstate Medical Centre, Brooklyn, NY, USA.
Clifford TaggartAirway Innate Immunity Research (AiiR) Group, Wellcome-Wolfson Institute for Experimental Medicine, School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast, Belfast, Northern Ireland, UK.
Sinéad WeldonAirway Innate Immunity Research (AiiR) Group, Wellcome-Wolfson Institute for Experimental Medicine, School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast, Belfast, Northern Ireland, UK.
Patrick GeraghtyDivision of Pulmonary & Critical Care Medicine, Department of Medicine, State University of New York Downstate Medical Centre, Brooklyn, NY, USA. Patrick.Geraghty@downstate.edu.ORCID http://orcid.org/0000-0003-1647-5505
State University of New York · USQueen's University Belfast · GB

Funding

Alpha-1 Foundation 614218Cystic Fibrosis Foundation WELDON18G0Flight Attendant Medical Research Institute CIA160005Medical Research Council MC_PC_13075Medical Research Council MR/P022847/1Rosetrees Trust A2450
6 · The paper itself

Abstract

Dysregulated expression and activity of cathepsin S (CTSS), a lysosomal protease and a member of the cysteine cathepsin protease family, is linked to the pathogenesis of multiple diseases, including a number of conditions affecting the lungs. Extracellular CTSS has potent elastase activity and by processing cytokines and host defense proteins, it also plays a role in the regulation of inflammation. CTSS has also been linked to G-coupled protein receptor activation and possesses an important intracellular role in major histocompatibility complex class II antigen presentation. Modulated CTSS activity is also associated with pulmonary disease comorbidities, such as cancer, cardiovascular disease, and diabetes. CTSS is expressed in a wide variety of immune cells and is biologically active at neutral pH. Herein, we review the significance of CTSS signaling in pulmonary diseases and associated comorbidities. We also discuss CTSS as a plausible therapeutic target and describe recent and current clinical trials examining CTSS inhibition as a means for treatment.

Indexed as

AnimalsAnti-Inflammatory AgentsCardiovascular DiseasesCathepsinsClinical Trials as TopicComorbidityHumansInflammation MediatorsLungLung DiseasesNeoplasmsSignal TransductionAnti-Inflammatory Agentscathepsin SCathepsinsInflammation Mediators

Identifiers

PMID32398133
PMCPMC7216426
OpenAlexW3025005589

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.