Evidence map›Paper›PMID 40047857›Full record

ReviewNaunyn-Schmiedeberg's archives of pharmacology2025

Targeting CXCR2 signaling in inflammatory lung diseases: neutrophil-driven inflammation and emerging therapies.

Md Sadique Hussain, Ahsas Goyal, Kavita Goyal, Renuka Jyothi S, Jayshree Nellore, Moyad Shahwan, A Rekha, Haider Ali, Muralikrishnan Dhanasekaran, Ronan MacLoughlin and 2 more

Abstract readReview
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In one paragraph

Review in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

  1. Review
  2. Galectin-9Aging cell · 2026
    Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Current pharmaceutical design · 2026
    Review
  9. Review
  10. Review
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  12. 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

12 authors.

Md Sadique HussainUttaranchal Institute of Pharmaceutical Sciences, Uttaranchal University, Dehradun, India.
Ahsas GoyalInstitute of Pharmaceutical Research, GLA University, Mathura, U.P, India.
Kavita GoyalDepartment of Biotechnology, Graphic Era (Deemed to Be University), Clement Town, 248002, Dehradun, India.
Renuka Jyothi SDepartment of Biotechnology and Genetics, Jain (Deemed-to-Be) University, Bengaluru, Karnataka, 560069, India.
Jayshree NelloreDepartment of Biotechnology, Sathyabama Institute of Science and Technology, Chennai, Tamil Nadu, India.
Moyad ShahwanCentre of Medical and Bio-Allied Health Sciences Research, Ajman University, Ajman, United Arab Emirates.
A RekhaDr. D. Y. Patil Medical College, Hospital and Research Centre, Pimpri, Pune, India.
Haider AliCentre for Global Health Research, Saveetha Medical College, Saveetha Institute of Medical and Technical Sciences, Saveetha University, Chennai, India.
Muralikrishnan DhanasekaranDepartment of Drug Discovery and Development, Harrison College of Pharmacy, Auburn University, Auburn, AL, USA.
Ronan MacLoughlinAerogen Ltd, Galway Business Park, Galway, Ireland.
Kamal DuaFaculty of Health, Australian Research Centre in Complementary and Integrative Medicine, University of Technology Sydney, Ultimo, Australia.
Gaurav GuptaCentre of Medical and Bio-Allied Health Sciences Research, Ajman University, Ajman, United Arab Emirates. gaurav.gupta@chitkara.edu.in.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory lung diseases (ILDs) such as asthma, acute respiratory distress syndrome, bronchiectasis, chronic obstructive pulmonary disease, COVID-19, cystic fibrosis, and lung cancer impose a substantial worldwide healthcare impact. The pathophysiology of these disorders is primarily influenced by the involvement of neutrophils, which are crucial triggers in the natural immune reaction. Neutrophils participate in pulmonary inflammation and tissue destruction. When neutrophils are activated and recruited, they migrate to inflammatory lung tissues via the chemokine receptor CXCR2. This study explores how neutrophils, directed by CXCR2 signaling, participate in the inflammatory environment in the lung, inducing tissue injury and the development of illness. We investigate both the functional and structural features of CXCR2, emphasizing its relationship with ligands such as IL-8 (CXCL8) and GRO-α (CXCL1) and its involvement in ILDs. The article also explores novel treatment approaches that focus on CXCR2, such as the use of small molecule antagonists. These compounds can regulate neutrophil behavior and reduce signs of the illness. The study provides a detailed analysis of current clinical studies and the results of inhibiting CXCR2, specifically looking at the effectiveness and safety of these new medicines. This study seeks to deliver a thorough analysis of the important function of neutrophils and CXCR2 in ILDs, as well as the possibility of CXCR2-targeted therapeutics to enhance clinical outcomes.

Indexed as

Lung DiseasesNeutrophilsReceptors, Interleukin-8BAnimalsCOVID-19HumansInflammationMolecular Targeted TherapySignal TransductionCXCR2 protein, humanReceptors, Interleukin-8BBronchiectasisChronic obstructive pulmonary diseaseCOVID-19CXCR2ILDsNeutrophils

Identifiers

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.