The influence of perivascular adipose tissue on vascular homeostasis.

Theodora Szasz, Gisele Facholi Bomfim, R Clinton Webb

Research output: Contribution to journalReview article

81 Citations (Scopus)

Abstract

The perivascular adipose tissue (PVAT) is now recognized as an active contributor to vascular function. Adipocytes and stromal cells contained within PVAT are a source of an ever-growing list of molecules with varied paracrine effects on the underlying smooth muscle and endothelial cells, including adipokines, cytokines, reactive oxygen species, and gaseous compounds. Their secretion is regulated by systemic or local cues and modulates complex processes, including vascular contraction and relaxation, smooth muscle cell proliferation and migration, and vascular inflammation. Recent evidence demonstrates that metabolic and cardiovascular diseases alter the morphological and secretory characteristics of PVAT, with notable consequences. In obesity and diabetes, the expanded PVAT contributes to vascular insulin resistance. PVAT-derived cytokines may influence key steps of atherogenesis. The physiological anticontractile effect of PVAT is severely diminished in hypertension. Above all, a common denominator of the PVAT dysfunction in all these conditions is the immune cell infiltration, which triggers the subsequent inflammation, oxidative stress, and hypoxic processes to promote vascular dysfunction. In this review, we discuss the currently known mechanisms by which the PVAT influences blood vessel function. The important discoveries in the study of PVAT that have been made in recent years need to be further advanced, to identify the mechanisms of the anticontractile effects of PVAT, to explore the vascular-bed and species differences in PVAT function, to understand the regulation of PVAT secretion of mediators, and finally, to uncover ways to ameliorate cardiovascular disease by targeting therapeutic approaches to PVAT.

Original languageEnglish (US)
Pages (from-to)105-116
Number of pages12
JournalUnknown Journal
Volume9
StatePublished - Jan 1 2013
Externally publishedYes

Fingerprint

Blood Vessels
Adipose Tissue
Homeostasis
Smooth Muscle Myocytes
Cardiovascular Diseases
Cytokines
Inflammation
Adipokines
Metabolic Diseases
Stromal Cells
Adipocytes
Vascular Resistance
Cell Movement
Cues
Insulin Resistance
Reactive Oxygen Species
Atherosclerosis
Oxidative Stress
Endothelial Cells
Obesity

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Hematology
  • Public Health, Environmental and Occupational Health
  • Cardiology and Cardiovascular Medicine
  • Pharmacology (medical)

Cite this

The influence of perivascular adipose tissue on vascular homeostasis. / Szasz, Theodora; Bomfim, Gisele Facholi; Webb, R Clinton.

In: Unknown Journal, Vol. 9, 01.01.2013, p. 105-116.

Research output: Contribution to journalReview article

Szasz, Theodora ; Bomfim, Gisele Facholi ; Webb, R Clinton. / The influence of perivascular adipose tissue on vascular homeostasis. In: Unknown Journal. 2013 ; Vol. 9. pp. 105-116.
@article{3144282f8d8c44f888fd7f3dd4b57b0c,
title = "The influence of perivascular adipose tissue on vascular homeostasis.",
abstract = "The perivascular adipose tissue (PVAT) is now recognized as an active contributor to vascular function. Adipocytes and stromal cells contained within PVAT are a source of an ever-growing list of molecules with varied paracrine effects on the underlying smooth muscle and endothelial cells, including adipokines, cytokines, reactive oxygen species, and gaseous compounds. Their secretion is regulated by systemic or local cues and modulates complex processes, including vascular contraction and relaxation, smooth muscle cell proliferation and migration, and vascular inflammation. Recent evidence demonstrates that metabolic and cardiovascular diseases alter the morphological and secretory characteristics of PVAT, with notable consequences. In obesity and diabetes, the expanded PVAT contributes to vascular insulin resistance. PVAT-derived cytokines may influence key steps of atherogenesis. The physiological anticontractile effect of PVAT is severely diminished in hypertension. Above all, a common denominator of the PVAT dysfunction in all these conditions is the immune cell infiltration, which triggers the subsequent inflammation, oxidative stress, and hypoxic processes to promote vascular dysfunction. In this review, we discuss the currently known mechanisms by which the PVAT influences blood vessel function. The important discoveries in the study of PVAT that have been made in recent years need to be further advanced, to identify the mechanisms of the anticontractile effects of PVAT, to explore the vascular-bed and species differences in PVAT function, to understand the regulation of PVAT secretion of mediators, and finally, to uncover ways to ameliorate cardiovascular disease by targeting therapeutic approaches to PVAT.",
author = "Theodora Szasz and Bomfim, {Gisele Facholi} and Webb, {R Clinton}",
year = "2013",
month = "1",
day = "1",
language = "English (US)",
volume = "9",
pages = "105--116",
journal = "Handbook of Behavioral Neuroscience",
issn = "0003-1348",
publisher = "JAI Press",

}

TY - JOUR

T1 - The influence of perivascular adipose tissue on vascular homeostasis.

AU - Szasz, Theodora

AU - Bomfim, Gisele Facholi

AU - Webb, R Clinton

PY - 2013/1/1

Y1 - 2013/1/1

N2 - The perivascular adipose tissue (PVAT) is now recognized as an active contributor to vascular function. Adipocytes and stromal cells contained within PVAT are a source of an ever-growing list of molecules with varied paracrine effects on the underlying smooth muscle and endothelial cells, including adipokines, cytokines, reactive oxygen species, and gaseous compounds. Their secretion is regulated by systemic or local cues and modulates complex processes, including vascular contraction and relaxation, smooth muscle cell proliferation and migration, and vascular inflammation. Recent evidence demonstrates that metabolic and cardiovascular diseases alter the morphological and secretory characteristics of PVAT, with notable consequences. In obesity and diabetes, the expanded PVAT contributes to vascular insulin resistance. PVAT-derived cytokines may influence key steps of atherogenesis. The physiological anticontractile effect of PVAT is severely diminished in hypertension. Above all, a common denominator of the PVAT dysfunction in all these conditions is the immune cell infiltration, which triggers the subsequent inflammation, oxidative stress, and hypoxic processes to promote vascular dysfunction. In this review, we discuss the currently known mechanisms by which the PVAT influences blood vessel function. The important discoveries in the study of PVAT that have been made in recent years need to be further advanced, to identify the mechanisms of the anticontractile effects of PVAT, to explore the vascular-bed and species differences in PVAT function, to understand the regulation of PVAT secretion of mediators, and finally, to uncover ways to ameliorate cardiovascular disease by targeting therapeutic approaches to PVAT.

AB - The perivascular adipose tissue (PVAT) is now recognized as an active contributor to vascular function. Adipocytes and stromal cells contained within PVAT are a source of an ever-growing list of molecules with varied paracrine effects on the underlying smooth muscle and endothelial cells, including adipokines, cytokines, reactive oxygen species, and gaseous compounds. Their secretion is regulated by systemic or local cues and modulates complex processes, including vascular contraction and relaxation, smooth muscle cell proliferation and migration, and vascular inflammation. Recent evidence demonstrates that metabolic and cardiovascular diseases alter the morphological and secretory characteristics of PVAT, with notable consequences. In obesity and diabetes, the expanded PVAT contributes to vascular insulin resistance. PVAT-derived cytokines may influence key steps of atherogenesis. The physiological anticontractile effect of PVAT is severely diminished in hypertension. Above all, a common denominator of the PVAT dysfunction in all these conditions is the immune cell infiltration, which triggers the subsequent inflammation, oxidative stress, and hypoxic processes to promote vascular dysfunction. In this review, we discuss the currently known mechanisms by which the PVAT influences blood vessel function. The important discoveries in the study of PVAT that have been made in recent years need to be further advanced, to identify the mechanisms of the anticontractile effects of PVAT, to explore the vascular-bed and species differences in PVAT function, to understand the regulation of PVAT secretion of mediators, and finally, to uncover ways to ameliorate cardiovascular disease by targeting therapeutic approaches to PVAT.

UR - http://www.scopus.com/inward/record.url?scp=84885572444&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84885572444&partnerID=8YFLogxK

M3 - Review article

VL - 9

SP - 105

EP - 116

JO - Handbook of Behavioral Neuroscience

JF - Handbook of Behavioral Neuroscience

SN - 0003-1348

ER -