Evidence map›Paper›PMID 34610470›Full record

ArticleBiochimica et biophysica acta. Molecular and cell biology of lipids2022

PLD1 promotes reactive oxygen species production in vascular smooth muscle cells and injury-induced neointima formation.

Ming Cai, Ziqing Wang, Thi Thu Trang Luu, Dakai Zhang, Brian Finke, Jingquan He, Li Wei Rachel Tay, Gilbert Di Paolo, Guangwei Du

Abstract read
In one paragraph

Article in Biochimica et biophysica acta. Molecular and cell biology of lipids, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 53% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. 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

9 authors at 3 institutions in 2 countries.

Ming CaiDepartment of Integrative Biology and Pharmacology, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA; Department of Gastrointestinal Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, Hubei Province, China.
Ziqing WangDepartment of Integrative Biology and Pharmacology, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
Thi Thu Trang LuuDepartment of Integrative Biology and Pharmacology, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA; Biochemistry and Cell Biology Program, MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences, Houston, TX 77030, USA.
Dakai ZhangDepartment of Integrative Biology and Pharmacology, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
Brian FinkeDepartment of Integrative Biology and Pharmacology, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
Jingquan HeDepartment of Integrative Biology and Pharmacology, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
Li Wei Rachel TayDepartment of Integrative Biology and Pharmacology, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
Gilbert Di PaoloDepartment of Pathology and Cell Biology, Columbia University Medical Center, New York, NY 10032, USA.
Guangwei DuDepartment of Integrative Biology and Pharmacology, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA. Electronic address: guangwei.du@uth.tmc.edu.
The University of Texas Health Science Center at Houston · USColumbia University Irving Medical Center · USThe University of Texas MD Anderson Cancer Center · US

Funding

American Heart Association-American Stroke Association 19TPA34910051
6 · The paper itself

Abstract

Phospholipase D (PLD) generates the signaling lipid phosphatidic acid (PA) and has been known to mediate proliferation signal in vascular smooth muscle cells (VSMCs). However, it remains unclear how PLD contributes to vascular diseases. VSMC proliferation directly contributes to the development and progression of cardiovascular disease, such as atherosclerosis and restenosis after angioplasty. Using the mouse carotid artery ligation model, we find that deletion of Pld1 gene inhibits neointima formation of the injuried blood vessels. PLD1 deficiency reduces the proliferation of VSMCs in both injured artery and primary cultures through the inhibition of ERK1/2 and AKT signals. Immunohistochemical staining of injured artery and flow cytometry analysis of VSMCs shows a reduction of the levels of reactive oxygen species (ROS) in Pld1

Indexed as

AnimalsAtherosclerosisCarotid ArteriesCarotid Artery InjuriesDisease Models, AnimalHumansMiceMuscle, Smooth, VascularMyocytes, Smooth MuscleNeointimaPhospholipase DReactive Oxygen SpeciesPhospholipase Dphospholipase D1Reactive Oxygen SpeciesNeointimaPLD1ProliferationVSMC

Identifiers

PMID34610470
PMCPMC11960192
OpenAlexW3204702866

What Socratic 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 Socratic graph.