Immune mechanisms in heart failure

Elevated levels of circulating pro‐inflammatory biomarkers in patients with both ischaemic and non‐ischaemic heart failure (HF) correlate with disease severity and prognosis. Experimental studies have shown activation of immune response mechanisms in the heart to provoke cardiac adverse remodelling...

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Published inEuropean journal of heart failure Vol. 19; no. 11; pp. 1379 - 1389
Main Authors Zhang, Yingying, Bauersachs, Johann, Langer, Harald F.
Format Journal Article
LanguageEnglish
Published Oxford, UK John Wiley & Sons, Ltd 01.11.2017
Subjects
Animals
Antigen presenting cells
Biomarkers - metabolism
Disease Progression
Heart failure
Heart Failure - immunology
Heart Failure - metabolism
Heart Failure - physiopathology
Humans
Immune response
Immunity, Innate
Inflammation
Inflammation - immunology
Inflammation - metabolism
Stroke Volume - physiology
Heart failure
Antigen presenting cells
Inflammation
Immune response
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Abstract Elevated levels of circulating pro‐inflammatory biomarkers in patients with both ischaemic and non‐ischaemic heart failure (HF) correlate with disease severity and prognosis. Experimental studies have shown activation of immune response mechanisms in the heart to provoke cardiac adverse remodelling and cause left ventricular dysfunction. Consequently, most of the clinical trials targeting elements of the immune response in HF attempted to modulate the inflammatory response. Surprisingly, clinical studies targeting immune effectors were either neutral or even increased pre‐specified clinical endpoints, and some studies resulted in worsening of HF. This review discusses immune mediators involved in the pathogenesis and progression of HF and potential therapeutic applications targeting inflammation in HF. Besides more obvious settings featuring immune activation such as inflammatory or ischaemic cardiomyopathy, the relevance of immune activation in acute or chronic HF of other origins, including volume overload or valvular heart disease, is highlighted. Understanding how cell‐specific and molecular mechanisms of the immune response interfere with cardiac remodelling in HF may open new avenues to design biomarkers or druggable targets.
AbstractList Elevated levels of circulating pro-inflammatory biomarkers in patients with both ischaemic and non-ischaemic heart failure (HF) correlate with disease severity and prognosis. Experimental studies have shown activation of immune response mechanisms in the heart to provoke cardiac adverse remodelling and cause left ventricular dysfunction. Consequently, most of the clinical trials targeting elements of the immune response in HF attempted to modulate the inflammatory response. Surprisingly, clinical studies targeting immune effectors were either neutral or even increased pre-specified clinical endpoints, and some studies resulted in worsening of HF. This review discusses immune mediators involved in the pathogenesis and progression of HF and potential therapeutic applications targeting inflammation in HF. Besides more obvious settings featuring immune activation such as inflammatory or ischaemic cardiomyopathy, the relevance of immune activation in acute or chronic HF of other origins, including volume overload or valvular heart disease, is highlighted. Understanding how cell-specific and molecular mechanisms of the immune response interfere with cardiac remodelling in HF may open new avenues to design biomarkers or druggable targets.
Elevated levels of circulating pro-inflammatory biomarkers in patients with both ischaemic and non-ischaemic heart failure (HF) correlate with disease severity and prognosis. Experimental studies have shown activation of immune response mechanisms in the heart to provoke cardiac adverse remodelling and cause left ventricular dysfunction. Consequently, most of the clinical trials targeting elements of the immune response in HF attempted to modulate the inflammatory response. Surprisingly, clinical studies targeting immune effectors were either neutral or even increased pre-specified clinical endpoints, and some studies resulted in worsening of HF. This review discusses immune mediators involved in the pathogenesis and progression of HF and potential therapeutic applications targeting inflammation in HF. Besides more obvious settings featuring immune activation such as inflammatory or ischaemic cardiomyopathy, the relevance of immune activation in acute or chronic HF of other origins, including volume overload or valvular heart disease, is highlighted. Understanding how cell-specific and molecular mechanisms of the immune response interfere with cardiac remodelling in HF may open new avenues to design biomarkers or druggable targets.Elevated levels of circulating pro-inflammatory biomarkers in patients with both ischaemic and non-ischaemic heart failure (HF) correlate with disease severity and prognosis. Experimental studies have shown activation of immune response mechanisms in the heart to provoke cardiac adverse remodelling and cause left ventricular dysfunction. Consequently, most of the clinical trials targeting elements of the immune response in HF attempted to modulate the inflammatory response. Surprisingly, clinical studies targeting immune effectors were either neutral or even increased pre-specified clinical endpoints, and some studies resulted in worsening of HF. This review discusses immune mediators involved in the pathogenesis and progression of HF and potential therapeutic applications targeting inflammation in HF. Besides more obvious settings featuring immune activation such as inflammatory or ischaemic cardiomyopathy, the relevance of immune activation in acute or chronic HF of other origins, including volume overload or valvular heart disease, is highlighted. Understanding how cell-specific and molecular mechanisms of the immune response interfere with cardiac remodelling in HF may open new avenues to design biomarkers or druggable targets.
Author Bauersachs, Johann
Langer, Harald F.
Zhang, Yingying
Author_xml – sequence: 1
  givenname: Yingying
  surname: Zhang
  fullname: Zhang, Yingying
  organization: Qingdao University
– sequence: 2
  givenname: Johann
  surname: Bauersachs
  fullname: Bauersachs, Johann
  organization: Hannover Medical School
– sequence: 3
  givenname: Harald F.
  surname: Langer
  fullname: Langer, Harald F.
  email: harald.langer@med.uni-tuebingen.de
  organization: Eberhard Karls University Tuebingen
BackLink https://www.ncbi.nlm.nih.gov/pubmed/28891154$$D View this record in MEDLINE/PubMed
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ISSN 1388-9842
1879-0844
IngestDate Fri Jul 11 12:18:25 EDT 2025
Mon Jul 21 05:42:05 EDT 2025
Tue Jul 01 01:54:17 EDT 2025
Thu Apr 24 22:58:27 EDT 2025
Wed Jan 22 16:50:04 EST 2025
IsPeerReviewed true
IsScholarly true
Issue 11
Keywords Heart failure
Antigen presenting cells
Inflammation
Immune response
Language English
License http://onlinelibrary.wiley.com/termsAndConditions#vor
2017 The Authors. European Journal of Heart Failure © 2017 European Society of Cardiology.
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PublicationTitle European journal of heart failure
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Snippet Elevated levels of circulating pro‐inflammatory biomarkers in patients with both ischaemic and non‐ischaemic heart failure (HF) correlate with disease severity...
Elevated levels of circulating pro-inflammatory biomarkers in patients with both ischaemic and non-ischaemic heart failure (HF) correlate with disease severity...
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SubjectTerms Animals
Antigen presenting cells
Biomarkers - metabolism
Disease Progression
Heart failure
Heart Failure - immunology
Heart Failure - metabolism
Heart Failure - physiopathology
Humans
Immune response
Immunity, Innate
Inflammation
Inflammation - immunology
Inflammation - metabolism
Stroke Volume - physiology
Title Immune mechanisms in heart failure
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fejhf.942
https://www.ncbi.nlm.nih.gov/pubmed/28891154
https://www.proquest.com/docview/1937764352
Volume 19
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