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Thrombospondin-1: Multiple Paths to Inflammation

Inflammation is a defensive process against tissue injury. Once this self-protective strategy is initiated, an effective resolution of the process is crucial to avoid major and unnecessary tissue damage. If the underlying event inducing inflammation is not addressed and homeostasis is not restored,...

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Detalles Bibliográficos
Autores principales: Lopez-Dee, Zenaida, Pidcock, Kenneth, Gutierrez, Linda S.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3134184/
https://www.ncbi.nlm.nih.gov/pubmed/21765615
http://dx.doi.org/10.1155/2011/296069
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author Lopez-Dee, Zenaida
Pidcock, Kenneth
Gutierrez, Linda S.
author_facet Lopez-Dee, Zenaida
Pidcock, Kenneth
Gutierrez, Linda S.
author_sort Lopez-Dee, Zenaida
collection PubMed
description Inflammation is a defensive process against tissue injury. Once this self-protective strategy is initiated, an effective resolution of the process is crucial to avoid major and unnecessary tissue damage. If the underlying event inducing inflammation is not addressed and homeostasis is not restored, this process can become chronic and lead to angiogenesis and carcinogenesis. Thrombospondin-1 (TSP-1) is a matricellular protein involved in angiogenesis, cancer, and inflammation. The effects of TSP-1 have been studied in many preclinical tumor models, and mimetic peptides are being tested in cancer clinical trials. However, the molecular mechanisms explaining its role in inflammatory processes are not well understood. This paper will discuss the role of TSP-1 in inflammation and its interaction with key receptors that may explain its functions in that process. Recent literature will be reviewed showing novel mechanisms by which this multifaceted protein could modulate the inflammatory process and impact its resolution.
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spelling pubmed-31341842011-07-15 Thrombospondin-1: Multiple Paths to Inflammation Lopez-Dee, Zenaida Pidcock, Kenneth Gutierrez, Linda S. Mediators Inflamm Review Article Inflammation is a defensive process against tissue injury. Once this self-protective strategy is initiated, an effective resolution of the process is crucial to avoid major and unnecessary tissue damage. If the underlying event inducing inflammation is not addressed and homeostasis is not restored, this process can become chronic and lead to angiogenesis and carcinogenesis. Thrombospondin-1 (TSP-1) is a matricellular protein involved in angiogenesis, cancer, and inflammation. The effects of TSP-1 have been studied in many preclinical tumor models, and mimetic peptides are being tested in cancer clinical trials. However, the molecular mechanisms explaining its role in inflammatory processes are not well understood. This paper will discuss the role of TSP-1 in inflammation and its interaction with key receptors that may explain its functions in that process. Recent literature will be reviewed showing novel mechanisms by which this multifaceted protein could modulate the inflammatory process and impact its resolution. Hindawi Publishing Corporation 2011 2011-07-03 /pmc/articles/PMC3134184/ /pubmed/21765615 http://dx.doi.org/10.1155/2011/296069 Text en Copyright © 2011 Zenaida Lopez-Dee et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Lopez-Dee, Zenaida
Pidcock, Kenneth
Gutierrez, Linda S.
Thrombospondin-1: Multiple Paths to Inflammation
title Thrombospondin-1: Multiple Paths to Inflammation
title_full Thrombospondin-1: Multiple Paths to Inflammation
title_fullStr Thrombospondin-1: Multiple Paths to Inflammation
title_full_unstemmed Thrombospondin-1: Multiple Paths to Inflammation
title_short Thrombospondin-1: Multiple Paths to Inflammation
title_sort thrombospondin-1: multiple paths to inflammation
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3134184/
https://www.ncbi.nlm.nih.gov/pubmed/21765615
http://dx.doi.org/10.1155/2011/296069
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