Evidence map›Paper›PMID 35002373›Full record

ReviewSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society2021

Current views in chronic obstructive pulmonary disease pathogenesis and management.

Ahmed J Alfahad, Mai M Alzaydi, Ahmad M Aldossary, Abdullah A Alshehri, Fahad A Almughem, Nada M Zaidan, Essam A Tawfik

Open access · hybridAbstract readReview
In one paragraph

Review in Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 5% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
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  12. Animal models and mechanisms of tobacco smoke-induced chronic obstructive pulmonary disease (COPD).Journal of toxicology and environmental health. Part B, Critical reviews · 2023
    Review
  13. Review
  14. 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

7 authors at 1 institution in 1 country.

Ahmed J AlfahadNational Center of Biotechnology, Life Science and Environment Research Institute, King Abdulaziz City for Science and Technology (KACST), P.O. Box 6086, Riyadh 11442, Saudi Arabia.
Mai M AlzaydiNational Center of Biotechnology, Life Science and Environment Research Institute, King Abdulaziz City for Science and Technology (KACST), P.O. Box 6086, Riyadh 11442, Saudi Arabia.
Ahmad M AldossaryNational Center of Biotechnology, Life Science and Environment Research Institute, King Abdulaziz City for Science and Technology (KACST), P.O. Box 6086, Riyadh 11442, Saudi Arabia.
Abdullah A AlshehriNational Center of Biotechnology, Life Science and Environment Research Institute, King Abdulaziz City for Science and Technology (KACST), P.O. Box 6086, Riyadh 11442, Saudi Arabia.
Fahad A AlmughemNational Center of Biotechnology, Life Science and Environment Research Institute, King Abdulaziz City for Science and Technology (KACST), P.O. Box 6086, Riyadh 11442, Saudi Arabia.
Nada M ZaidanCenter of Excellence in Biomedicine, Joint Centers of Excellence Program, King Abdulaziz City for Science and Technology (KACST), P.O. Box 6086, Riyadh 11442, Saudi Arabia.
Essam A TawfikNational Center of Biotechnology, Life Science and Environment Research Institute, King Abdulaziz City for Science and Technology (KACST), P.O. Box 6086, Riyadh 11442, Saudi Arabia.
King Abdulaziz City for Science and Technology · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) is a progressive lung dysfunction caused mainly by inhaling toxic particles and cigarette smoking (CS). The continuous exposure to ruinous molecules can lead to abnormal inflammatory responses, permanent damages to the respiratory system, and irreversible pathological changes. Other factors, such as genetics and aging, influence the development of COPD. In the last decade, accumulating evidence suggested that mitochondrial alteration, including mitochondrial DNA damage, increased mitochondrial reactive oxygen species (ROS), abnormal autophagy, and apoptosis, have been implicated in the pathogenesis of COPD. The alteration can also extend to epigenetics, namely DNA methylation, histone modification, and non-coding RNA. This review will discuss the recent progressions in COPD pathology, pathophysiology, and molecular pathways. More focus will be shed on mitochondrial and epigenetic variations related to COPD development and the role of nanomedicine as a potential tool for the prevention and treatment of this disease.

Indexed as

Chronic obstructive pulmonary disease (COPD)Epigenetic alterationsMitochondrial alterationsMitochondrial epigeneticsNanomedicine

Identifiers

PMID35002373
PMCPMC8720819
OpenAlexW3209123151

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.