Evidence map›Paper›PMID 36744401›Full record

ArticleExpert opinion on therapeutic targets2023

Airway smooth muscle in contractility and remodeling of asthma: potential drug target mechanisms.

Latifa Khalfaoui, Christina M Pabelick

Open access · greenAbstract read
In one paragraph

Article in Expert opinion on therapeutic targets, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.9field-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

25 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. [Pathological roles of lipid metabolism disorders in asthma and related intervention strategies].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026
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  19. Role of STIM1 in stretch-induced signaling in human airway smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  20. Downregulation of protein phosphatase 2Aα in asthmatic airway smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2024
    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

2 authors at 2 institutions in 1 country.

Latifa KhalfaouiDepartments of Anesthesiology & Perioperative Medicine Mayo Clinic, Rochester, MN, USA.
Christina M PabelickDepartments of Anesthesiology & Perioperative Medicine Mayo Clinic, Rochester, MN, USA.
Mayo Clinic in Arizona · USMayo Clinic in Florida · US

Funding

Neurotrophins in the LungR01HL088029 · NHLBI · MAYO CLINIC ROCHESTER · PI PRAKASH, Y. S. · 2009 to 2022
$5.9M
Nicotine, Airway Smooth Muscle and AsthmaR01HL142061 · NHLBI · MAYO CLINIC ROCHESTER · PI PABELICK, CHRISTINA MARIA, PRAKASH, Y. S. · 2019 to 2022
$2.0M
NHLBI NIH HHS R01 HL088029NHLBI NIH HHS R01 HL142061
6 · The paper itself

Abstract

introductionAsthma is characterized by enhanced airway contractility and remodeling where airway smooth muscle (ASM) plays a key role, modulated by inflammation. Understanding the mechanisms by which ASM contributes to these features of asthma is essential for the development of novel asthma therapies. AREAS COVERED: Inflammation in asthma contributes to a multitude of changes within ASM including enhanced airway contractility, proliferation, and fibrosis. Altered intracellular calcium ([Ca EXPERT OPINION: ASM plays a significant role in multiple features of asthma. Increased ASM contractility contributes to hyperresponsiveness, while altered ASM proliferation and extracellular matrix production promote airway remodeling both influenced by inflammation of asthma and conversely even influencing the local inflammatory milieu. While standard therapies such as corticosteroids or biologics target inflammation, cytokines, or their receptors to alleviate asthma symptoms, these approaches do not address the underlying contribution of ASM to hyperresponsiveness and particularly remodeling. Therefore, novel therapies for asthma need to target abnormal contractility mechanisms in ASM and/or the contribution of ASM to remodeling, particularly in asthmatics resistant to current therapies.

Indexed as

AsthmaAirway RemodelingFibrosisHumansInflammationMuscle, SmoothRespiratory Systemairwayairway hyperreactivityairway smooth musclecalciumdrug targetsfibrosisLungproliferation

Identifiers

PMID36744401
PMCPMC10208413
OpenAlexW4319295008

What Socratic 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 Socratic graph.