Evidence map›Paper›PMID 31170951›Full record

ArticleBMC pulmonary medicine2019

Ursolic acid alleviates airway-vessel remodeling and muscle consumption in cigarette smoke-induced emphysema rats.

Li Lin, Gang Hou, Dan Han, Yan Yin, Jian Kang, Qiuyue Wang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC pulmonary medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Mitochondrial dysfunction: roles in skeletal muscle atrophy.Journal of translational medicine · 2023
    Review
  5. Article
  6. Article
  7. Article
  8. Molecules (Basel, Switzerland) · 2022
    Article
  9. Review
  10. Review
  11. Turkish journal of chemistry · 2022
    Article
  12. Review
  13. 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

6 authors at 2 institutions in 1 country.

Li LinInstitute of Respiratory Disease, The First Hospital of China Medical University, No. 155 Nanjing North Street, Shenyang, 110001, China.
Gang HouInstitute of Respiratory Disease, The First Hospital of China Medical University, No. 155 Nanjing North Street, Shenyang, 110001, China.
Dan HanInstitute of Respiratory Disease, The First Hospital of China Medical University, No. 155 Nanjing North Street, Shenyang, 110001, China.
Yan YinInstitute of Respiratory Disease, The First Hospital of China Medical University, No. 155 Nanjing North Street, Shenyang, 110001, China.
Jian KangInstitute of Respiratory Disease, The First Hospital of China Medical University, No. 155 Nanjing North Street, Shenyang, 110001, China.
Qiuyue WangInstitute of Respiratory Disease, The First Hospital of China Medical University, No. 155 Nanjing North Street, Shenyang, 110001, China. qywang2002@hotmail.com.
China Medical University · CNFirst Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThis study assessed the effects of ursolic acid (UA) on airway-vessel remodeling and muscle atrophy in cigarette smoke (CS)-induced emphysema rats and investigated potential underlying mechanisms.

methodsEmphysema was induced in a rat model with 3 months of CS exposure. Histology and immunohistochemistry (IHC) stains were used to assess airway-vessel remodeling and muscle atrophy-associated changes. Levels of cleaved-caspase3, 8-OHdG, and S100A4 were measured in airways and associated vessels to evaluate cell apoptosis, oxidant stress, epithelial-to-mesenchymal transition (EMT), and endothelial-to-mesenchymal transition (EndMT)-associated factors. Western blot and/or IHC analyses were performed to measure transforming growth factor-beta 1(TGF-β1)/Smad2.3, alpha-smooth muscle actin (α-SMA), and insulin-like growth factor 1 (IGF1) expression. We also gave cultured HBE and HUVEC cells Cigarette Smoke Extract (CSE) administration and UA intervention. Using Western blot method to measure TGF-β1/Smad2.3, α-SMA, S100A4, and IGF1 molecules expression.

resultsUA decreased oxidant stress and cell apoptosis in airway and accompanying vascular walls of cigarette smoke-induced emphysema model rats. UA alleviated EMT, EndMT, changes associated with airway-vessel remodeling and muscle atrophy. The UA effects were associated with IGF1 and TGF-β1/Smad2.3 pathways.

conclusionsUA reduced EMT, EndMT, airway-vessel remodeling, and musculi soleus atrophy in CS-induced emphysema model rats at least partly through IGF1 and TGF-β1/Smad2.3 signaling pathways.

Indexed as

Airway RemodelingAnimalsAtrophyCigarette SmokingCyclooxygenase InhibitorsEpithelial-Mesenchymal TransitionInsulin-Like Growth Factor IMaleMuscle, SkeletalPulmonary EmphysemaRatsRats, WistarSignal TransductionSmad2 ProteinSmokeTransforming Growth Factor beta1Cyclooxygenase InhibitorsInsulin-Like Growth Factor ISmad2 ProteinSmokeTransforming Growth Factor beta1TriterpenesUrsolic Acid

Identifiers

PMID31170951
PMCPMC6555740
OpenAlexW2948753187

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.