Evidence map›Paper›PMID 35047522›Full record

ReviewFrontiers in medicine2021

Dysregulated Cell Signaling in Pulmonary Emphysema.

Chih-Ru Lin, Karim Bahmed, Beata Kosmider

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

8 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. A translational view of airway epithelial dysfunction in COPD.European respiratory review : an official journal of the European Respiratory Society · 2025
    Review
  5. Review
  6. Article
  7. Review
  8. Review
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

3 authors at 1 institution in 1 country.

Chih-Ru LinDepartment of Microbiology, Immunology, and Inflammation, Temple University, Philadelphia, PA, United States.
Karim BahmedCenter for Inflammation and Lung Research, Temple University, Philadelphia, PA, United States.
Beata KosmiderDepartment of Microbiology, Immunology, and Inflammation, Temple University, Philadelphia, PA, United States.
Temple University · US

Funding

Regulation of alveolar epithelial regeneration by T cellsR01HL150587 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI KOSMIDER, BEATA, TIAN, YING · 2020 to 2023
$2.2M
Alveolar Epithelial Cell Dysfunction Induced By Flavored E-Cigarette AerosolsR01ES032081 · NIEHS · TEMPLE UNIV OF THE COMMONWEALTH · PI KOSMIDER, BEATA · 2020 to 2024
$1.9M
Cigarette smoke influences alveolar type II cell-derived exosomesR21ES030808 · NIEHS · TEMPLE UNIV OF THE COMMONWEALTH · PI BAHMED, KARIM · 2020 to 2021
$434k
NHLBI NIH HHS R01 HL150587NIEHS NIH HHS R01 ES032081NIEHS NIH HHS R21 ES030808
6 · The paper itself

Abstract

Pulmonary emphysema is characterized by the destruction of alveolar septa and irreversible airflow limitation. Cigarette smoking is the primary cause of this disease development. It induces oxidative stress and disturbs lung physiology and tissue homeostasis. Alveolar type II (ATII) cells have stem cell potential and can repair the denuded epithelium after injury; however, their dysfunction is evident in emphysema. There is no effective treatment available for this disease. Challenges in this field involve the large complexity of lung pathophysiological processes and gaps in our knowledge on the mechanisms of emphysema progression. It implicates dysregulation of various signaling pathways, including aberrant inflammatory and oxidative responses, defective antioxidant defense system, surfactant dysfunction, altered proteostasis, disrupted circadian rhythms, mitochondrial damage, increased cell senescence, apoptosis, and abnormal proliferation and differentiation. Also, genetic predispositions are involved in this disease development. Here, we comprehensively review studies regarding dysregulated cell signaling, especially in ATII cells, and their contribution to alveolar wall destruction in emphysema. Relevant preclinical and clinical interventions are also described.

Indexed as

alveolar epitheliumalveolar type II cellsemphysemalungoxidative stresstissue homeostasis

Identifiers

PMID35047522
PMCPMC8762198
OpenAlexW4206676572

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.