Vascular Smooth Muscle Cells

Dario F. Riascos-Bernal, Nicholas E.S. Sibinga

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

This chapter addresses extrinsic signals that affect vascular smooth muscle cell (SMC) phenotype and intrinsic cellular and molecular processes that affect SMC activities during atherogenesis. SMCs participate in all stages of atheroma formation. In the intima, monocytes differentiate into macrophages that phagocytose modified lipids and lipoprotein particles and become foam cells. Cytokines and growth factors such as platelet-derived growth factor (PDGF)-BB released from macrophages and foam cells induce dedifferentiation and migration of SMCs from media to intima. SMCs are centrally involved in the progression from early fatty streak to advanced fibrofatty atheroma. Plaque stability becomes critical as atherosclerosis progresses. SMCs support plaque stability by synthesizing extracellular matrix (ECM) proteins, lending mechanical strength to the fibrous cap overlying the plaque. SMC death is also important, as loss of SMCs limits ECM synthesis. At basal levels, autophagy recycles damaged cellular components and promotes survival, and therefore may serve to stabilize atheromas.

Original languageEnglish (US)
Title of host publicationAtherosclerosis: Risks, Mechanisms, and Therapies
PublisherWiley Blackwell
Pages117-128
Number of pages12
ISBN (Electronic)9781118828533
ISBN (Print)9781118285916
DOIs
StatePublished - Mar 27 2015

Fingerprint

Atherosclerotic Plaques
Vascular Smooth Muscle
Smooth Muscle Myocytes
Muscle
Foam Cells
Macrophages
Cells
Foams
Atherosclerosis
Cell Dedifferentiation
Extracellular Matrix Proteins
Autophagy
Cell death
Phagocytosis
Lipoproteins
Strength of materials
Cell Movement
Extracellular Matrix
Monocytes
Intercellular Signaling Peptides and Proteins

Keywords

  • Atherogenesis
  • Atheroma progression
  • Autophagy
  • Extracellular matrix (ECM)
  • Plaque stability
  • Platelet-derived growth factor (PDGF)
  • Vascular smooth muscle cell (SMC)

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Riascos-Bernal, D. F., & Sibinga, N. E. S. (2015). Vascular Smooth Muscle Cells. In Atherosclerosis: Risks, Mechanisms, and Therapies (pp. 117-128). Wiley Blackwell. https://doi.org/10.1002/9781118828533.ch10

Vascular Smooth Muscle Cells. / Riascos-Bernal, Dario F.; Sibinga, Nicholas E.S.

Atherosclerosis: Risks, Mechanisms, and Therapies. Wiley Blackwell, 2015. p. 117-128.

Research output: Chapter in Book/Report/Conference proceedingChapter

Riascos-Bernal, DF & Sibinga, NES 2015, Vascular Smooth Muscle Cells. in Atherosclerosis: Risks, Mechanisms, and Therapies. Wiley Blackwell, pp. 117-128. https://doi.org/10.1002/9781118828533.ch10
Riascos-Bernal DF, Sibinga NES. Vascular Smooth Muscle Cells. In Atherosclerosis: Risks, Mechanisms, and Therapies. Wiley Blackwell. 2015. p. 117-128 https://doi.org/10.1002/9781118828533.ch10
Riascos-Bernal, Dario F. ; Sibinga, Nicholas E.S. / Vascular Smooth Muscle Cells. Atherosclerosis: Risks, Mechanisms, and Therapies. Wiley Blackwell, 2015. pp. 117-128
@inbook{a282263600db47e89f5ebc14be2737f5,
title = "Vascular Smooth Muscle Cells",
abstract = "This chapter addresses extrinsic signals that affect vascular smooth muscle cell (SMC) phenotype and intrinsic cellular and molecular processes that affect SMC activities during atherogenesis. SMCs participate in all stages of atheroma formation. In the intima, monocytes differentiate into macrophages that phagocytose modified lipids and lipoprotein particles and become foam cells. Cytokines and growth factors such as platelet-derived growth factor (PDGF)-BB released from macrophages and foam cells induce dedifferentiation and migration of SMCs from media to intima. SMCs are centrally involved in the progression from early fatty streak to advanced fibrofatty atheroma. Plaque stability becomes critical as atherosclerosis progresses. SMCs support plaque stability by synthesizing extracellular matrix (ECM) proteins, lending mechanical strength to the fibrous cap overlying the plaque. SMC death is also important, as loss of SMCs limits ECM synthesis. At basal levels, autophagy recycles damaged cellular components and promotes survival, and therefore may serve to stabilize atheromas.",
keywords = "Atherogenesis, Atheroma progression, Autophagy, Extracellular matrix (ECM), Plaque stability, Platelet-derived growth factor (PDGF), Vascular smooth muscle cell (SMC)",
author = "Riascos-Bernal, {Dario F.} and Sibinga, {Nicholas E.S.}",
year = "2015",
month = "3",
day = "27",
doi = "10.1002/9781118828533.ch10",
language = "English (US)",
isbn = "9781118285916",
pages = "117--128",
booktitle = "Atherosclerosis: Risks, Mechanisms, and Therapies",
publisher = "Wiley Blackwell",

}

TY - CHAP

T1 - Vascular Smooth Muscle Cells

AU - Riascos-Bernal, Dario F.

AU - Sibinga, Nicholas E.S.

PY - 2015/3/27

Y1 - 2015/3/27

N2 - This chapter addresses extrinsic signals that affect vascular smooth muscle cell (SMC) phenotype and intrinsic cellular and molecular processes that affect SMC activities during atherogenesis. SMCs participate in all stages of atheroma formation. In the intima, monocytes differentiate into macrophages that phagocytose modified lipids and lipoprotein particles and become foam cells. Cytokines and growth factors such as platelet-derived growth factor (PDGF)-BB released from macrophages and foam cells induce dedifferentiation and migration of SMCs from media to intima. SMCs are centrally involved in the progression from early fatty streak to advanced fibrofatty atheroma. Plaque stability becomes critical as atherosclerosis progresses. SMCs support plaque stability by synthesizing extracellular matrix (ECM) proteins, lending mechanical strength to the fibrous cap overlying the plaque. SMC death is also important, as loss of SMCs limits ECM synthesis. At basal levels, autophagy recycles damaged cellular components and promotes survival, and therefore may serve to stabilize atheromas.

AB - This chapter addresses extrinsic signals that affect vascular smooth muscle cell (SMC) phenotype and intrinsic cellular and molecular processes that affect SMC activities during atherogenesis. SMCs participate in all stages of atheroma formation. In the intima, monocytes differentiate into macrophages that phagocytose modified lipids and lipoprotein particles and become foam cells. Cytokines and growth factors such as platelet-derived growth factor (PDGF)-BB released from macrophages and foam cells induce dedifferentiation and migration of SMCs from media to intima. SMCs are centrally involved in the progression from early fatty streak to advanced fibrofatty atheroma. Plaque stability becomes critical as atherosclerosis progresses. SMCs support plaque stability by synthesizing extracellular matrix (ECM) proteins, lending mechanical strength to the fibrous cap overlying the plaque. SMC death is also important, as loss of SMCs limits ECM synthesis. At basal levels, autophagy recycles damaged cellular components and promotes survival, and therefore may serve to stabilize atheromas.

KW - Atherogenesis

KW - Atheroma progression

KW - Autophagy

KW - Extracellular matrix (ECM)

KW - Plaque stability

KW - Platelet-derived growth factor (PDGF)

KW - Vascular smooth muscle cell (SMC)

UR - http://www.scopus.com/inward/record.url?scp=85015828379&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85015828379&partnerID=8YFLogxK

U2 - 10.1002/9781118828533.ch10

DO - 10.1002/9781118828533.ch10

M3 - Chapter

AN - SCOPUS:85015828379

SN - 9781118285916

SP - 117

EP - 128

BT - Atherosclerosis: Risks, Mechanisms, and Therapies

PB - Wiley Blackwell

ER -