Evidence map›Paper›PMID 26871724›Full record

ArticlePloS one2016

Key Role of ROS in the Process of 15-Lipoxygenase/15-Hydroxyeicosatetraenoiccid-Induced Pulmonary Vascular Remodeling in Hypoxia Pulmonary Hypertension.

Qian Li, Min Mao, Yanli Qiu, Gaofeng Liu, Tingting Sheng, Xiufeng Yu, Shuang Wang, Daling Zhu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Article
  3. Linking Lipid Metabolism and Immune Function: New Insights into Chronic Respiratory Diseases.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025
    Review
  4. Review
  5. Review
  6. Article
  7. Pulmonary Vascular Remodeling in Pulmonary Hypertension.Journal of personalized medicine · 2023
    Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
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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

8 authors at 2 institutions in 2 countries.

Qian LiDepartment of Pharmaceutical Analysis, College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang Province, China.
Min MaoDepartment of Pathophysiology, Harbin Medical University-Daqing, Daqing, Heilongjiang Province, China.
Yanli QiuDepartment of Pharmaceutical Analysis, College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang Province, China.
Gaofeng LiuDepartment of Pharmacy, the Second Affiliated Hospital, Harbin Medical University, Harbin, Heilongjiang Province, China.
Tingting ShengDepartment of Pathophysiology, Harbin Medical University-Daqing, Daqing, Heilongjiang Province, China.
Xiufeng YuDepartment of Pathophysiology, Harbin Medical University-Daqing, Daqing, Heilongjiang Province, China.
Shuang WangDepartment of Pharmaceutical Analysis, College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang Province, China.
Daling ZhuDepartment of Pathophysiology, Harbin Medical University-Daqing, Daqing, Heilongjiang Province, China.
Harbin Medical University · CNDaqing City People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously reported that 15-lipoxygenase (15-LO) and its metabolite 15-hydroxyeicosatetraenoic acid (15-HETE) were up-regulated in pulmonary arterial cells from both pulmonary artery hypertension patients and hypoxic rats and that these factors mediated the progression of pulmonary hypertension (PH) by affecting the proliferation and apoptosis of pulmonary arterial (PA) cells. However, the underlying mechanisms of the remodeling induced by 15-HETE have remained unclear. As reactive oxygen species (ROS) and 15-LO are both induced by hypoxia, it is possible that ROS are involved in the events of hypoxia-induced 15-LO expression that lead to PH. We employed immunohistochemistry, tube formation assays, bromodeoxyuridine (BrdU) incorporation assays, and cell cycle analyses to explore the role of ROS in the process of 15-HETE-mediated hypoxic pulmonary hypertension (HPH). We found that exogenous 15-HETE facilitated the generation of ROS and that this effect was mainly localized to mitochondria. In particular, the mitochondrial electron transport chain and nicotinamide-adenine dinucleotide phosphate oxidase 4 (Nox4) were responsible for the significant 15-HETE-stimulated increase in ROS production. Moreover, ROS induced by 15-HETE stimulated endothelial cell (EC) migration and promoted pulmonary artery smooth muscle cell (PASMC) proliferation under hypoxia via the p38 MAPK pathway. These results indicated that 15-HETE-regulated ROS mediated hypoxia-induced pulmonary vascular remodeling (PVR) via the p38 MAPK pathway.

Indexed as

Vascular RemodelingAnimalsArachidonate 15-LipoxygenaseCattleCells, CulturedFemaleHumansHydroxyeicosatetraenoic AcidsHypertension, PulmonaryHypoxiaLungNADPH Oxidase 4NADPH Oxidasesp38 Mitogen-Activated Protein KinasesRatsRats, Wistar15-hydroxy-5,8,11,13-eicosatetraenoic acidArachidonate 15-LipoxygenaseHydroxyeicosatetraenoic AcidsNADPH Oxidase 4NADPH OxidasesNOX4 protein, humanNox4 protein, ratp38 Mitogen-Activated Protein KinasesReactive Oxygen Species

Identifiers

PMID26871724
PMCPMC4752324
OpenAlexW2254045887

What OpenQuestion holds

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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.