Related Experiment Video
Updated: Jun 14, 2026

Murine Aortic Crush Injury: An Efficient In Vivo Model of Smooth Muscle Cell Proliferation and Endothelial Function
Published on: June 11, 2017
Involvement of ERK1/2 kinase in insulin-and thrombin-stimulated vascular smooth muscle cell proliferation
Esma R Isenovic1, Mamdouh H Kedees, Mohamed A Haidara
1Vinca Institute of Nuclear Sciences, University of Belgrade, Laboratory for Molecular Genetics and Radiobiology, Belgrade, Serbia. isenovic@yahoo.com
Abstract:
It is well recognized that the proliferation of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of various vascular diseases, including atherosclerosis and hypertension. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42- and 44-kDa isoforms (ERK1/2) participate in the cellular mitogenic machinery triggered by several VSMCs activators, including insulin (INS) and thrombin (Thr). However, understanding of the intracellular signal transduction pathways involved is incomplete. This review considers the recent findings in INS and Thr signaling mechanisms that modulate the proliferation of VSMCs with particular emphasis on the ERK1/2 signaling pathway, an important mediator of VSMCs hypertrophy and vascular disease. Moreover, because the ERK1/2 pathway have been acknowledged as an important mediator of VSMCs hypertrophy, ERK1/2 is identified as a key target for novel therapeutic interventions to minimize irreversible tissue damage associated with hypertension and atherosclerosis.
Insights
Vascular smooth muscle cell (VSMC) proliferation drives vascular diseases. This review highlights how insulin and thrombin signaling, particularly the ERK1/2 pathway, mediate VSMC hypertrophy and offers therapeutic targets for atherosclerosis and hypertension.
Area of Science:
- Biochemistry
- Cell Biology
- Cardiovascular Research
Background:
- Vascular smooth muscle cell (VSMC) proliferation is central to vascular diseases like atherosclerosis and hypertension.
- Extracellular signal-regulated kinases (ERKs), specifically ERK1/2, are known to be involved in VSMC mitogenesis.
- Intracellular signaling pathways regulating VSMC proliferation remain incompletely understood.
Purpose of the Study:
- To review recent findings on insulin (INS) and thrombin (Thr) signaling mechanisms.
- To emphasize the role of the ERK1/2 signaling pathway in VSMC proliferation and hypertrophy.
- To identify ERK1/2 as a potential therapeutic target for vascular diseases.
Main Methods:
- Literature review of recent studies on VSMC signaling.
- Focus on intracellular pathways activated by INS and Thr.
- Analysis of the ERK1/2 pathway's role in VSMC hypertrophy.
Main Results:
- INS and Thr activate signaling cascades that promote VSMC proliferation.
- The ERK1/2 pathway is a key mediator of INS- and Thr-induced VSMC hypertrophy.
- Understanding these pathways is crucial for developing new treatments.
Conclusions:
- The ERK1/2 pathway is a critical mediator of VSMC hypertrophy.
- Targeting the ERK1/2 pathway presents a promising therapeutic strategy for hypertension and atherosclerosis.
- Further research into INS and Thr signaling can lead to novel interventions for vascular disease.
Related Concept Videos
PI3K/mTOR/AKT Signaling Pathway
Intracellular Signaling Affects Focal Adhesions
Some...
MAPK Signaling Cascades
Regulation of Angiogenesis and Blood Supply
cAMP-dependent Protein Kinase Pathways
TGF - β Signaling Pathway

