Evidence map›Paper›PMID 24468195›Full record

ReviewRespiratory medicine2014

Complement components as potential therapeutic targets for asthma treatment.

Mohammad Afzal Khan, Mark R Nicolls, Besiki Surguladze, Ismail Saadoun

Open access · bronzeAbstract readReview
In one paragraph

Review in Respiratory medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 15% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Effective delivery of miR-511-3p with mannose-decorated exosomes with RNA nanoparticles confers protection against asthma.Journal of controlled release : official journal of the Controlled Release Society · 2024
    Article
  8. Article
  9. Complement System Inhibitory Drugs in a Zebrafish (International journal of molecular sciences · 2023
    Article
  10. Article
  11. Genes · 2022
    Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

4 authors at 2 institutions in 2 countries.

Mohammad Afzal KhanDepartment of Applied Biology, College of Sciences, University of Sharjah, Sharjah, United Arab Emirates. Electronic address: makhan@sharjah.ac.ae.
Mark R NicollsDivision of Pulmonary and Critical Care Medicine, VA Palo Health Care System, Stanford University, School of Medicine, Palo Alto, CA, USA.
Besiki SurguladzeInnovative Bio-Medical Technologies Ltd, Toronto, Canada.
Ismail SaadounDepartment of Applied Biology, College of Sciences, University of Sharjah, Sharjah, United Arab Emirates.
University of Sharjah · AEVA Palo Alto Health Care System · US

Funding

The Cellular Response to Elafin in PAHP01HL108797 · NHLBI · STANFORD UNIVERSITY · PI NOLAN, GARRY P · 2011 to 2021
$19.7M
Critical Role for Microvasculature in Airway TransplantationR01HL095686 · NHLBI · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI NICOLLS, MARK ROBERT · 2010 to 2022
$4.7M
NHLBI NIH HHS P01 HL108797NHLBI NIH HHS R01 HL095686
6 · The paper itself

Abstract

Asthma is the most common respiratory disorder, and is characterized by distal airway inflammation and hyperresponsiveness. This disease challenges human health because of its increasing prevalence, severity, morbidity, and the lack of a proper and complete cure. Asthma is characterized by T(H)2-skewed inflammation with elevated pulmonary levels of IL-4, IL-5, and IL-13 levels. Although there are early forays into targeting T(H)2 immunity, less-specific corticosteroid therapy remains the immunomodulator of choice. Innate immune injury mediated by complement components also act as potent mediators of the allergic inflammatory responses and offer a new and exciting possibility for asthma immunotherapy. The complement cascade consists of a number of plasma- and membrane-bound proteins, and the cleavage products of these proteins (C3 and C5) regulate the magnitude of adaptive immune responses. Complement protein are responsible for many pathophysiological features of asthma, including inflammatory cell infiltration, mucus secretion, increases in vascular permeability, and smooth muscle cell contraction. This review highlights the complement-mediated injury during asthma inflammation, and how blockade of active complement mediators may have therapeutic application.

Indexed as

Anti-Asthmatic AgentsAsthmaComplement C3aComplement C5aComplement Inactivating AgentsComplement System ProteinsHumansImmunity, InnateMolecular Targeted TherapyAnti-Asthmatic AgentsComplement C3aComplement C5aComplement Inactivating AgentsComplement System ProteinsAnaphylatoxinsAsthmaComplement mediated injury

Identifiers

PMID24468195
PMCPMC4011641
OpenAlexW2154257183

What OpenQuestion holds

Textmetadata
LicenceTDM
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.