Evidence map›Paper›PMID 28458526›Full record

ReviewInternational journal of chronic obstructive pulmonary disease2017

Mitochondrial alterations during oxidative stress in chronic obstructive pulmonary disease.

Ying Jiang, Xiaoqin Wang, Daode Hu

Open access · goldAbstract readReview
In one paragraph

Review in International journal of chronic obstructive pulmonary disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
5.1field-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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. [Overexpressing NDUFA13 and CRIP1 improves B cell injury and lung Lesions in COPD mouse models].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
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  16. Sex-specific lung inflammation and mitochondrial damage in a model of electronic cigarette exposure in asthma.American journal of physiology. Lung cellular and molecular physiology · 2023
    Article
  17. Article
  18. Review
  19. Review
  20. Role of autophagy in lung diseases and ageing.European respiratory review : an official journal of the European Respiratory Society · 2022
    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 2 institutions in 1 country.

Ying JiangDepartment of Clinical Pharmacology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
Xiaoqin WangDepartment of Clinical Pharmacology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
Daode HuDepartment of Clinical Pharmacology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
Shanghai First People's Hospital · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The high incidence of chronic obstructive pulmonary disease (COPD), one of the most prevalent diseases worldwide, has attracted growing attention. Cigarette smoking is considered a major contributory factor in the pathogenesis and progression of COPD due to the tremendous oxidative burden that it causes, which induces an oxidant/antioxidant imbalance. Excessive oxidation induced by the excessive generation of mitochondrial reactive oxygen species disturbs the antioxidant systems and plays an important role in triggering and promoting chronic inflammation of airways. Given that mitochondria is one of the main sites of reactive oxygen species production by the oxidative phosphorylation process, oxidative stress may affect mitochondrial function by changing its structure and morphology and by affecting a series of mitochondrial proteins. In particular, PTEN-induced putative kinase 1/Parkin and p62 play critical roles in mitophagy. During the process, the Akt ubiquitin E3 ligase is an important mediator associated with cigarette smoke exposure-induced pulmonary endothelial cell death and dysfunction. Thus, understanding the underlying mechanisms of the signaling pathway may provide important information regarding the therapeutic treatment of COPD by application of alternative PTEN-induced putative kinase 1 targets or ubiquitin E3 ligase.

Indexed as

Oxidative StressAnimalsAntioxidantsHumansLungMitochondriaMitophagyPhosphorylationPulmonary Disease, Chronic ObstructiveReactive Oxygen SpeciesSequestosome-1 ProteinSignal TransductionUbiquitin-Protein LigasesAntioxidantsparkin proteinReactive Oxygen SpeciesSequestosome-1 ProteinUbiquitin-Protein Ligaseschronic obstructive pulmonary diseasemitochondrial fission/fusionmitophagyreactive nitrogen stressreactive oxidative stress

Identifiers

PMID28458526
PMCPMC5402882
OpenAlexW2607249259

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.