Evidence map›Paper›PMID 39000009›Full record

ArticleInternational journal of molecular sciences2024

Yohimbine Inhibits PDGF-Induced Vascular Smooth Muscle Cell Proliferation and Migration via FOXO3a Factor.

Leejin Lim, Hyeonhwa Kim, Jihye Jeong, Sung Hee Han, Young-Bob Yu, Heesang Song

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Multifaced Nature of Yohimbine-A Promising Therapeutic Potential or a Risk?International journal of molecular sciences · 2024
    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.

Leejin LimAdvanced Cancer Controlling Research Center, Chosun University, Gwangju 61452, Republic of Korea.
Hyeonhwa KimDepartment of Biomedical Sciences, Chosun University Graduate School, Gwangju 61452, Republic of Korea.
Jihye JeongDepartment of Biomedical Sciences, Chosun University Graduate School, Gwangju 61452, Republic of Korea.
Sung Hee HanInstitute of Human Behavior & Genetics, Biomedical Research Center, Korea University, Seoul 02841, Republic of Korea.
Young-Bob YuDepartment of Paramedicine, Nambu University, Gwangju 62271, Republic of Korea.ORCID 0000-0001-7785-5988
Heesang SongAdvanced Cancer Controlling Research Center, Chosun University, Gwangju 61452, Republic of Korea.ORCID 0000-0003-0891-2429

Funding

Chosun University 2024National Research Foundation of Korea NRF-2021R1I1A3051564
6 · The paper itself

Abstract

Yohimbine (YHB) has been reported to possess anti-inflammatory, anticancer, and cardiac function-enhancing properties. Additionally, it has been reported to inhibit the proliferation, migration, and neointimal formation of vascular smooth muscle cells (VSMCs) induced by platelet-derived growth factor (PDGF) stimulation by suppressing the phospholipase C-gamma 1 pathway. However, the transcriptional regulatory mechanism of YHB controlling the behavior of VSMCs is not fully understood. In this study, YHB downregulated the expression of cell cycle regulatory proteins, such as proliferating cell nuclear antigen (PCNA), cyclin D1, cyclin-dependent kinase 4 (CDK4), and cyclin E, by modulating the transcription factor FOXO3a in VSMCs induced by PDGF. Furthermore, YHB decreased p-38 and mTOR phosphorylation in a dose-dependent manner. Notably, YHB significantly reduced the phosphorylation at Y397 and Y925 sites of focal adhesion kinase (FAK), and this effect was greater at the Y925 site than Y397. In addition, the expression of paxillin, a FAK-associated protein known to bind to the Y925 site of FAK, was significantly reduced by YHB treatment in a dose-dependent manner. A pronounced reduction in the migration and proliferation of VSMCs was observed following co-treatment of YHB with mTOR or p38 inhibitors. In conclusion, this study shows that YHB inhibits the PDGF-induced proliferation and migration of VSMCs by regulating the transcription factor FOXO3a and the mTOR/p38/FAK signaling pathway. Therefore, YHB may be a potential therapeutic candidate for preventing and treating cardiovascular diseases such as atherosclerosis and vascular restenosis.

Indexed as

Cell MovementCell ProliferationForkhead Box Protein O3Muscle, Smooth, VascularMyocytes, Smooth MusclePlatelet-Derived Growth FactorYohimbineAnimalsCells, CulturedFocal Adhesion Kinase 1Malep38 Mitogen-Activated Protein KinasesPaxillinPhosphorylationRatsRats, Sprague-DawleyFocal Adhesion Kinase 1Forkhead Box Protein O3FOXO3 protein, ratp38 Mitogen-Activated Protein KinasesPaxillinPlatelet-Derived Growth FactorTOR Serine-Threonine KinasesYohimbineFOXO3amigrationmTORproliferationvascular smooth muscle cellsyohimbine

Identifiers

PMID39000009
PMCPMC11240894

What Socratic 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 Socratic graph.