Role of Inflammatory Cell Subtypes in Heart Failure

Inflammation is a well-known feature of heart failure. Studies have shown that while some inflammation is required for repair during injury and is protective, prolonged inflammation leads to myocardial remodeling and apoptosis of cardiac myocytes. Various types of immune cells are implicated in myoc...

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Main Authors: Derek Strassheim, Edward C. Dempsey, Evgenia Gerasimovskaya, Kurt Stenmark, Vijaya Karoor
Format: Article
Language:English
Published: Hindawi Limited 2019-01-01
Series:Journal of Immunology Research
Online Access:http://dx.doi.org/10.1155/2019/2164017
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spelling doaj-1220b3ea826e483fbb5f8f0c83583d9b2020-11-25T00:44:54ZengHindawi LimitedJournal of Immunology Research2314-88612314-71562019-01-01201910.1155/2019/21640172164017Role of Inflammatory Cell Subtypes in Heart FailureDerek Strassheim0Edward C. Dempsey1Evgenia Gerasimovskaya2Kurt Stenmark3Vijaya Karoor4Cardiovascular Pulmonary Research Laboratory, University of Colorado Denver, Aurora CO, USACardiovascular Pulmonary Research Laboratory, University of Colorado Denver, Aurora CO, USACardiovascular Pulmonary Research Laboratory, University of Colorado Denver, Aurora CO, USACardiovascular Pulmonary Research Laboratory, University of Colorado Denver, Aurora CO, USACardiovascular Pulmonary Research Laboratory, University of Colorado Denver, Aurora CO, USAInflammation is a well-known feature of heart failure. Studies have shown that while some inflammation is required for repair during injury and is protective, prolonged inflammation leads to myocardial remodeling and apoptosis of cardiac myocytes. Various types of immune cells are implicated in myocardial inflammation and include neutrophils, macrophages, eosinophils, mast cells, natural killer cells, T cells, and B cells. Recent clinical trials have targeted inflammatory cascades as therapy for heart failure with limited success. A better understanding of the temporal course of the infiltration of the different immune cells and their contribution to the inflammatory process may improve the success for therapy. This brief review outlines the major cell types involved in heart failure, and some of their actions are summarized in the supplementary figure.http://dx.doi.org/10.1155/2019/2164017
collection DOAJ
language English
format Article
sources DOAJ
author Derek Strassheim
Edward C. Dempsey
Evgenia Gerasimovskaya
Kurt Stenmark
Vijaya Karoor
spellingShingle Derek Strassheim
Edward C. Dempsey
Evgenia Gerasimovskaya
Kurt Stenmark
Vijaya Karoor
Role of Inflammatory Cell Subtypes in Heart Failure
Journal of Immunology Research
author_facet Derek Strassheim
Edward C. Dempsey
Evgenia Gerasimovskaya
Kurt Stenmark
Vijaya Karoor
author_sort Derek Strassheim
title Role of Inflammatory Cell Subtypes in Heart Failure
title_short Role of Inflammatory Cell Subtypes in Heart Failure
title_full Role of Inflammatory Cell Subtypes in Heart Failure
title_fullStr Role of Inflammatory Cell Subtypes in Heart Failure
title_full_unstemmed Role of Inflammatory Cell Subtypes in Heart Failure
title_sort role of inflammatory cell subtypes in heart failure
publisher Hindawi Limited
series Journal of Immunology Research
issn 2314-8861
2314-7156
publishDate 2019-01-01
description Inflammation is a well-known feature of heart failure. Studies have shown that while some inflammation is required for repair during injury and is protective, prolonged inflammation leads to myocardial remodeling and apoptosis of cardiac myocytes. Various types of immune cells are implicated in myocardial inflammation and include neutrophils, macrophages, eosinophils, mast cells, natural killer cells, T cells, and B cells. Recent clinical trials have targeted inflammatory cascades as therapy for heart failure with limited success. A better understanding of the temporal course of the infiltration of the different immune cells and their contribution to the inflammatory process may improve the success for therapy. This brief review outlines the major cell types involved in heart failure, and some of their actions are summarized in the supplementary figure.
url http://dx.doi.org/10.1155/2019/2164017
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