Evidence map›Paper›PMID 31323822›Full record

ReviewInternational journal of molecular sciences2019

Defining Bronchial Asthma with Phosphoinositide 3-Kinase Delta Activation: Towards Endotype-Driven Management.

Jae Seok Jeong, Jong Seung Kim, So Ri Kim, Yong Chul Lee

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 33 citations in OpenAlex.

  1. Mechanisms and therapeutic strategies of asthma: from bench to bedside.Signal transduction and targeted therapy · 2026
    Review
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  12. Design, Synthesis, and Development of pyrazolo[1,5-Pharmaceuticals (Basel, Switzerland) · 2022
    Article
  13. Extracellular Vesicles and Asthma-More Than Just a Co-Existence.International journal of molecular sciences · 2021
    Review
  14. Review
  15. 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 1 institution in 1 country.

Jae Seok JeongDepartment of Internal Medicine, Research Center for Pulmonary Disorders, Chonbuk National University Medical School, Jeonju 54907, Korea.
Jong Seung KimResearch Institute of Clinical Medicine of Chonbuk National University-Biomedical Research Institute of Chonbuk National University Hospital, Jeonju 54907, Korea.
So Ri KimDepartment of Internal Medicine, Research Center for Pulmonary Disorders, Chonbuk National University Medical School, Jeonju 54907, Korea.ORCID 0000-0002-6074-9158
Yong Chul LeeDepartment of Internal Medicine, Research Center for Pulmonary Disorders, Chonbuk National University Medical School, Jeonju 54907, Korea. leeyc@jbnu.ac.kr.
Jeonbuk National University Hospital · KR

Funding

Ministry of Science and ICT of South Korea NRF-2017R1A2A1A05000747
6 · The paper itself

Abstract

Phosphoinositide 3-kinase (PI3K) pathways play a critical role in orchestrating the chronic inflammation and the structural changes of the airways in patients with asthma. Recently, a great deal of progress has been made in developing selective and effective PI3K-targeted therapies on the basis of a vast amount of studies on the roles of specific PI3K isoforms and fine-tuned modulators of PI3Ks in a particular disease context. In particular, the pivotal roles of delta isoform of class I PI3Ks (PI3K-δ) in CD4-positive type 2 helper T cells-dominant disorders such as asthma have been consistently reported since the early investigations. Furthermore, there has been great advancement in our knowledge of the implications of PI3K-δ in various facets of allergic inflammation. This has involved the airway epithelial interface, adaptive T and B cells, potent effector cells (eosinophils and neutrophils), and, more recently, subcellular organelles (endoplasmic reticulum and mitochondria) and cytoplasmic innate immune receptors such as NLRP3 inflammasome, all of which make this PI3K isoform an important druggable target for treating asthma. Defining subpopulations of asthma patients with PI3K-δ activation, namely PI3K-δ-driven asthma endotype, may therefore provide us with a novel framework for the treatment of the disease, particularly for corticosteroid-resistant severe form, an important unresolved aspect of the current asthma management. In this review, we specifically summarize the recent advancement of our knowledge on the critical roles of PI3K-δ in the pathogenesis of bronchial asthma.

Indexed as

AnimalsAsthmaHumansPhosphatidylinositol 3-KinasesPrecision MedicineSignal TransductionPhosphatidylinositol 3-Kinasesbronchial asthmaendotypephosphoinositide 3-kinase deltaprecision medicine

Identifiers

PMID31323822
PMCPMC6679152
OpenAlexW2958233381

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.