Evidence map›Paper›PMID 33174444›Full record

ReviewAmerican journal of physiology. Lung cellular and molecular physiology2021

Why new biology must be uncovered to advance therapeutic strategies for chronic obstructive pulmonary disease.

Jennifer M K Nguyen, Douglas N Robinson, Venkataramana K Sidhaye

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Lung cellular and molecular physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 10% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
  2. Predominant lung cDC2 phenotype in cigarette smoke-exposed mice favors polarization of IL-17-producing CD4American journal of physiology. Lung cellular and molecular physiology · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Relationship Between ACSL4-Mediated Ferroptosis and Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2023
    Article
  9. Article
  10. Human lung cDC1 drive increased perforin-mediated NK cytotoxicity in chronic obstructive pulmonary disease.American journal of physiology. Lung cellular and molecular physiology · 2021
    Article
  11. 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

3 authors at 1 institution in 1 country.

Jennifer M K NguyenDepartment of Cell Biology, Johns Hopkins School of Medicine, Baltimore, Maryland.
Douglas N RobinsonDepartment of Cell Biology, Johns Hopkins School of Medicine, Baltimore, Maryland.ORCID 0000-0003-1236-4891
Venkataramana K SidhayeDepartment of Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland.
Johns Hopkins University · US

Funding

The Biochemical Basis for the Mechanics of CytokinesisR01GM066817 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI ROBINSON, DOUGLAS N · 2003 to 2025
$7.3M
Role of E-cadherin in modulating airway epithelial function and parenchymal remodelingR01HL151107 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI SIDHAYE, VENKATARAMANA K · 2020 to 2023
$2.4M
Actin-myosin contractility promotes the development of chronic bronchitisR01HL124099 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI SIDHAYE, VENKATARAMANA K · 2017 to 2021
$2.1M
Characterization of Adenine Nucleotide Translocase (ANT) and Actin-Interacting Protein 1 (AIP1) as Protectors Against Cigarette SmokeF31HL145910 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI NGUYEN, JENNIFER · 2019 to 2021
$111k
NHLBI NIH HHS F31 HL145910NHLBI NIH HHS R01 HL124099NHLBI NIH HHS R01 HL151107NIGMS NIH HHS R01 GM066817
6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) is characterized by the destruction of alveolar tissue (in emphysema) and airway remodeling (leading to chronic bronchitis), which cause difficulties in breathing. It is a growing public health concern with few therapeutic options that can reverse disease progression or mortality. This is in part because current treatments mainly focus on ameliorating symptoms induced by inflammatory pathways as opposed to curing disease. Hence, emerging research focused on upstream pathways are likely to be beneficial in the development of efficient therapeutics to address the root causes of disease. Some of these pathways include mitochondrial function, cytoskeletal structure and maintenance, and airway hydration, which are all affected by toxins that contribute to COPD. Because of the complexity of COPD and unknown targets for disease onset, simpler model organisms have proved to be useful tools in identifying disease-relevant pathways and targets. This review summarizes COPD pathology, current treatments, and therapeutic discovery research, with a focus on the aforementioned pathways that can advance the therapeutic landscape of COPD.

Indexed as

Signal TransductionAnimalsHumansPulmonary Disease, Chronic Obstructiveairway and alveolar epitheliumcigarette smokecytoskeletonmitochondriamodel organisms

Identifiers

PMID33174444
PMCPMC7847061
OpenAlexW3100805188

What OpenQuestion holds

Textmetadata
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.