Perivascular adipose tissue inflammation in vascular disease
Perivascular adipose tissue (PVAT) plays a critical role in the pathogenesis of cardiovascular disease. In vascular pathologies, perivascular adipose tissue increases in volume and becomes dysfunctional, with altered cellular composition and molecular characteristics. PVAT dysfunction is characteriz...
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Veröffentlicht in: | British journal of pharmacology 2017-10, Vol.174 (20), p.3496-3513 |
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description | Perivascular adipose tissue (PVAT) plays a critical role in the pathogenesis of cardiovascular disease. In vascular pathologies, perivascular adipose tissue increases in volume and becomes dysfunctional, with altered cellular composition and molecular characteristics. PVAT dysfunction is characterized by its inflammatory character, oxidative stress, diminished production of vaso‐protective adipocyte‐derived relaxing factors and increased production of paracrine factors such as resistin, leptin, cytokines (IL‐6 and TNF‐α) and chemokines [RANTES (CCL5) and MCP‐1 (CCL2)]. These adipocyte‐derived factors initiate and orchestrate inflammatory cell infiltration including primarily T cells, macrophages, dendritic cells, B cells and NK cells. Protective factors such as adiponectin can reduce NADPH oxidase superoxide production and increase NO bioavailability in the vessel wall, while inflammation (e.g. IFN‐γ or IL‐17) induces vascular oxidases and eNOS dysfunction in the endothelium, vascular smooth muscle cells and adventitial fibroblasts. All of these events link the dysfunctional perivascular fat to vascular dysfunction. These mechanisms are important in the context of a number of cardiovascular disorders including atherosclerosis, hypertension, diabetes and obesity. Inflammatory changes in PVAT's molecular and cellular responses are uniquely different from classical visceral or subcutaneous adipose tissue or from adventitia, emphasizing the unique structural and functional features of this adipose tissue compartment. Therefore, it is essential to develop techniques for monitoring the characteristics of PVAT and assessing its inflammation. This will lead to a better understanding of the early stages of vascular pathologies and the development of new therapeutic strategies focusing on perivascular adipose tissue.
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This article is part of a themed section on Molecular Mechanisms Regulating Perivascular Adipose Tissue – Potential Pharmacological Targets? To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.20/issuetoc |
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Linked Articles
This article is part of a themed section on Molecular Mechanisms Regulating Perivascular Adipose Tissue – Potential Pharmacological Targets? To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.20/issuetoc</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1111/bph.13705</identifier><identifier>PMID: 28063251</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>Adipocytes ; Adiponectin ; Adipose tissue ; Adipose Tissue - physiopathology ; Animals ; Arteriosclerosis ; Beta cells ; Bioavailability ; Blood Vessels - physiopathology ; Chemokines ; Cytokines - physiology ; Dendritic cells ; Diabetes mellitus ; Endothelium ; Fibroblasts ; Humans ; Inflammation ; Inflammation - immunology ; Inflammation - physiopathology ; Interleukin 17 ; Interleukin 6 ; Leptin ; Lymphocytes ; Lymphocytes T ; Macrophages ; Molecular modelling ; Monocyte chemoattractant protein 1 ; Muscles ; NAD(P)H oxidase ; Oxidative stress ; Paracrine signalling ; RANTES ; Review ; Smooth muscle ; Structure-function relationships ; Superoxide ; Themed Section: Review ; Vascular Diseases - immunology ; Vascular Diseases - physiopathology</subject><ispartof>British journal of pharmacology, 2017-10, Vol.174 (20), p.3496-3513</ispartof><rights>2017 The British Pharmacological Society</rights><rights>2017 The British Pharmacological Society.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5095-e83fbf8a60bfc9229c125479d0fc7f85e45912e50a842ecb8256e787df18660d3</citedby><cites>FETCH-LOGICAL-c5095-e83fbf8a60bfc9229c125479d0fc7f85e45912e50a842ecb8256e787df18660d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5610164/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5610164/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,1427,27903,27904,45553,45554,46387,46811,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28063251$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nosalski, Ryszard</creatorcontrib><creatorcontrib>Guzik, Tomasz J</creatorcontrib><title>Perivascular adipose tissue inflammation in vascular disease</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>Perivascular adipose tissue (PVAT) plays a critical role in the pathogenesis of cardiovascular disease. In vascular pathologies, perivascular adipose tissue increases in volume and becomes dysfunctional, with altered cellular composition and molecular characteristics. PVAT dysfunction is characterized by its inflammatory character, oxidative stress, diminished production of vaso‐protective adipocyte‐derived relaxing factors and increased production of paracrine factors such as resistin, leptin, cytokines (IL‐6 and TNF‐α) and chemokines [RANTES (CCL5) and MCP‐1 (CCL2)]. These adipocyte‐derived factors initiate and orchestrate inflammatory cell infiltration including primarily T cells, macrophages, dendritic cells, B cells and NK cells. Protective factors such as adiponectin can reduce NADPH oxidase superoxide production and increase NO bioavailability in the vessel wall, while inflammation (e.g. IFN‐γ or IL‐17) induces vascular oxidases and eNOS dysfunction in the endothelium, vascular smooth muscle cells and adventitial fibroblasts. All of these events link the dysfunctional perivascular fat to vascular dysfunction. These mechanisms are important in the context of a number of cardiovascular disorders including atherosclerosis, hypertension, diabetes and obesity. Inflammatory changes in PVAT's molecular and cellular responses are uniquely different from classical visceral or subcutaneous adipose tissue or from adventitia, emphasizing the unique structural and functional features of this adipose tissue compartment. Therefore, it is essential to develop techniques for monitoring the characteristics of PVAT and assessing its inflammation. This will lead to a better understanding of the early stages of vascular pathologies and the development of new therapeutic strategies focusing on perivascular adipose tissue.
Linked Articles
This article is part of a themed section on Molecular Mechanisms Regulating Perivascular Adipose Tissue – Potential Pharmacological Targets? To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.20/issuetoc</description><subject>Adipocytes</subject><subject>Adiponectin</subject><subject>Adipose tissue</subject><subject>Adipose Tissue - physiopathology</subject><subject>Animals</subject><subject>Arteriosclerosis</subject><subject>Beta cells</subject><subject>Bioavailability</subject><subject>Blood Vessels - physiopathology</subject><subject>Chemokines</subject><subject>Cytokines - physiology</subject><subject>Dendritic cells</subject><subject>Diabetes mellitus</subject><subject>Endothelium</subject><subject>Fibroblasts</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inflammation - immunology</subject><subject>Inflammation - physiopathology</subject><subject>Interleukin 17</subject><subject>Interleukin 6</subject><subject>Leptin</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Macrophages</subject><subject>Molecular modelling</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Muscles</subject><subject>NAD(P)H oxidase</subject><subject>Oxidative stress</subject><subject>Paracrine signalling</subject><subject>RANTES</subject><subject>Review</subject><subject>Smooth muscle</subject><subject>Structure-function relationships</subject><subject>Superoxide</subject><subject>Themed Section: Review</subject><subject>Vascular Diseases - immunology</subject><subject>Vascular Diseases - physiopathology</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kU1LxDAQhoMouq4e_ANS8KKHapI2HwURVPyCBT3oOaTpRCP9WJPtiv_euF0XFZzLMMzDwwwvQnsEH5NYJ-X05ZhkArM1NCK54CnLJFlHI4yxSAmRcgtth_CKcVwKtom2qMQ8o4yM0OkDeDfXwfS19omu3LQLkMxcCD0krrW1bho9c10bh2TFVS6ADrCDNqyuA-wu-xg9XV89Xt6mk_ubu8vzSWoYLlgKMrOllZrj0pqC0sIQynJRVNgaYSWDnBWEAsNa5hRMKSnjIKSoLJGc4yobo7PBO-3LBioD7czrWk29a7T_UJ126vemdS_quZsrxgkmPI-Cw6XAd289hJlqXDBQ17qFrg-KSMZZIfACPfiDvna9b-N7ihQ55bzgNIvU0UAZ34Xgwa6OIVh9ZaJiJmqRSWT3f16_Ir9DiMDJALy7Gj7-N6mLh9tB-QkkdZXm</recordid><startdate>201710</startdate><enddate>201710</enddate><creator>Nosalski, Ryszard</creator><creator>Guzik, Tomasz J</creator><general>Blackwell Publishing Ltd</general><general>John Wiley and Sons Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7TK</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201710</creationdate><title>Perivascular adipose tissue inflammation in vascular disease</title><author>Nosalski, Ryszard ; Guzik, Tomasz J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5095-e83fbf8a60bfc9229c125479d0fc7f85e45912e50a842ecb8256e787df18660d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adipocytes</topic><topic>Adiponectin</topic><topic>Adipose tissue</topic><topic>Adipose Tissue - physiopathology</topic><topic>Animals</topic><topic>Arteriosclerosis</topic><topic>Beta cells</topic><topic>Bioavailability</topic><topic>Blood Vessels - physiopathology</topic><topic>Chemokines</topic><topic>Cytokines - physiology</topic><topic>Dendritic cells</topic><topic>Diabetes mellitus</topic><topic>Endothelium</topic><topic>Fibroblasts</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Inflammation - immunology</topic><topic>Inflammation - physiopathology</topic><topic>Interleukin 17</topic><topic>Interleukin 6</topic><topic>Leptin</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Macrophages</topic><topic>Molecular modelling</topic><topic>Monocyte chemoattractant protein 1</topic><topic>Muscles</topic><topic>NAD(P)H oxidase</topic><topic>Oxidative stress</topic><topic>Paracrine signalling</topic><topic>RANTES</topic><topic>Review</topic><topic>Smooth muscle</topic><topic>Structure-function relationships</topic><topic>Superoxide</topic><topic>Themed Section: Review</topic><topic>Vascular Diseases - immunology</topic><topic>Vascular Diseases - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nosalski, Ryszard</creatorcontrib><creatorcontrib>Guzik, Tomasz J</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nosalski, Ryszard</au><au>Guzik, Tomasz J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Perivascular adipose tissue inflammation in vascular disease</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>2017-10</date><risdate>2017</risdate><volume>174</volume><issue>20</issue><spage>3496</spage><epage>3513</epage><pages>3496-3513</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><abstract>Perivascular adipose tissue (PVAT) plays a critical role in the pathogenesis of cardiovascular disease. In vascular pathologies, perivascular adipose tissue increases in volume and becomes dysfunctional, with altered cellular composition and molecular characteristics. PVAT dysfunction is characterized by its inflammatory character, oxidative stress, diminished production of vaso‐protective adipocyte‐derived relaxing factors and increased production of paracrine factors such as resistin, leptin, cytokines (IL‐6 and TNF‐α) and chemokines [RANTES (CCL5) and MCP‐1 (CCL2)]. These adipocyte‐derived factors initiate and orchestrate inflammatory cell infiltration including primarily T cells, macrophages, dendritic cells, B cells and NK cells. Protective factors such as adiponectin can reduce NADPH oxidase superoxide production and increase NO bioavailability in the vessel wall, while inflammation (e.g. IFN‐γ or IL‐17) induces vascular oxidases and eNOS dysfunction in the endothelium, vascular smooth muscle cells and adventitial fibroblasts. All of these events link the dysfunctional perivascular fat to vascular dysfunction. These mechanisms are important in the context of a number of cardiovascular disorders including atherosclerosis, hypertension, diabetes and obesity. Inflammatory changes in PVAT's molecular and cellular responses are uniquely different from classical visceral or subcutaneous adipose tissue or from adventitia, emphasizing the unique structural and functional features of this adipose tissue compartment. Therefore, it is essential to develop techniques for monitoring the characteristics of PVAT and assessing its inflammation. This will lead to a better understanding of the early stages of vascular pathologies and the development of new therapeutic strategies focusing on perivascular adipose tissue.
Linked Articles
This article is part of a themed section on Molecular Mechanisms Regulating Perivascular Adipose Tissue – Potential Pharmacological Targets? To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.20/issuetoc</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>28063251</pmid><doi>10.1111/bph.13705</doi><tpages>18</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adipocytes Adiponectin Adipose tissue Adipose Tissue - physiopathology Animals Arteriosclerosis Beta cells Bioavailability Blood Vessels - physiopathology Chemokines Cytokines - physiology Dendritic cells Diabetes mellitus Endothelium Fibroblasts Humans Inflammation Inflammation - immunology Inflammation - physiopathology Interleukin 17 Interleukin 6 Leptin Lymphocytes Lymphocytes T Macrophages Molecular modelling Monocyte chemoattractant protein 1 Muscles NAD(P)H oxidase Oxidative stress Paracrine signalling RANTES Review Smooth muscle Structure-function relationships Superoxide Themed Section: Review Vascular Diseases - immunology Vascular Diseases - physiopathology |
title | Perivascular adipose tissue inflammation in vascular disease |
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