Evidence map›Paper›PMID 26617525›Full record

ReviewFrontiers in physiology2015

Molecular Regulation of Toll-like Receptors in Asthma and COPD.

Li Zuo, Kurt Lucas, Christopher A Fortuna, Chia-Chen Chuang, Thomas M Best

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 3% 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, 1 synthesis or guideline pooled it, 122 citations in OpenAlex.

  1. A molecular systems architecture of asthma.Frontiers in immunology · 2026
    Pooled it
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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

5 authors at 3 institutions in 2 countries.

Li ZuoRadiologic Sciences and Respiratory Therapy Division, The Ohio State University Wexner Medical Center, School of Health and Rehabilitation Sciences, The Ohio State University College of Medicine, Columbus, Ohio State University Columbus, OH, USA ; Interdisciplinary Biophysics Graduate Program, The Ohio State University Columbus, OH, USA.
Kurt LucasMultiphase Chemistry Department, Max Planck Institute for Chemistry Mainz, Germany.
Christopher A FortunaRadiologic Sciences and Respiratory Therapy Division, The Ohio State University Wexner Medical Center, School of Health and Rehabilitation Sciences, The Ohio State University College of Medicine, Columbus, Ohio State University Columbus, OH, USA.
Chia-Chen ChuangRadiologic Sciences and Respiratory Therapy Division, The Ohio State University Wexner Medical Center, School of Health and Rehabilitation Sciences, The Ohio State University College of Medicine, Columbus, Ohio State University Columbus, OH, USA ; Interdisciplinary Biophysics Graduate Program, The Ohio State University Columbus, OH, USA.
Thomas M BestDivision of Sports Medicine, Department of Family Medicine, Sports Health and Performance Institute, The Ohio State University Wexner Medical Center Columbus, OH, USA.
The Ohio State University Wexner Medical Center · USMax Planck Institute for Chemistry · DEThe Ohio State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Asthma and chronic obstructive pulmonary disease (COPD) have both been historically associated with significant morbidity and financial burden. These diseases can be induced by several exogenous factors, such as pathogen-associated molecular patterns (PAMPs) (e.g., allergens and microbes). Endogenous factors, including reactive oxygen species, and damage-associated molecular patterns (DAMPs) recognized by toll-like receptors (TLRs), can also result in airway inflammation. Asthma is characterized by the dominant presence of eosinophils, mast cells, and clusters of differentiation (CD)4(+) T cells in the airways, while COPD typically results in the excessive formation of neutrophils, macrophages, and CD8(+) T cells in the airways. In both asthma and COPD, in the respiratory tract, TLRs are the primary proteins of interest associated with the innate and adaptive immune responses; hence, multiple treatment options targeting TLRs are being explored in an effort to reduce the severity of the symptoms of these disorders. TLR-mediated pathways for both COPD and asthma have their similarities and differences with regards to cell types and the pro-inflammatory cytotoxins present in the airway. Because of the complex TLR cascade, a variety of treatments have been used to minimize airway hypersensitivity and promote bronchodilation. Although unsuccessful at completely alleviating COPD and severe asthmatic symptoms, new studies are focused on possible targets within the TLR cascade to ameliorate airway inflammation.

Indexed as

antioxidantDAMPPAMPpolymorphismreactive oxygen speciesTLR

Identifiers

PMID26617525
PMCPMC4637409
OpenAlexW2165410977

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.