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Inflammation and metabolic cardiomyopathy

Cardiovascular research, 2017-03, Vol.113 (4), p.389-398 [Peer Reviewed Journal]

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2017. For permissions, please email: journals.permissions@oup.com. ;ISSN: 0008-6363 ;EISSN: 1755-3245 ;DOI: 10.1093/cvr/cvx012 ;PMID: 28395010

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Title:
Inflammation and metabolic cardiomyopathy
Author: Nishida, Kazuhiko ; Otsu, Kinya
Subjects: Animals ; Autophagy ; Cardiomyopathies - immunology ; Cardiomyopathies - metabolism ; Cardiomyopathies - pathology ; Cardiomyopathies - physiopathology ; Humans ; Immunity, Innate ; Inflammation - immunology ; Inflammation - metabolism ; Inflammation - pathology ; Inflammation - physiopathology ; Inflammation Mediators - immunology ; Inflammation Mediators - metabolism ; Myocardium - immunology ; Myocardium - metabolism ; Myocardium - pathology ; Prognosis ; Signal Transduction
Is Part Of: Cardiovascular research, 2017-03, Vol.113 (4), p.389-398
Description: Excessive feeding is associated with an increase in the incidence of chronic metabolic diseases, such as obesity, insulin resistance, and type 2 diabetes. Metabolic disturbance induces chronic low-grade inflammation in metabolically-important organs, such as the liver and adipose tissue. Many of the inflammatory signalling pathways are directly triggered by nutrients. The pro-inflammatory mediators in adipocytes and macrophages infiltrating adipose tissue promote both local and systemic pro-inflammatory status. Metabolic cardiomyopathy is a chronic metabolic disease characterized by structural and functional alterations and interstitial fibrosis without coronary artery disease or hypertension. In the early stage of metabolic cardiomyopathy, metabolic disturbance is not accompanied by substantial changes in myocardial structure and cardiac function. However, metabolic disturbance induces subcellular low-grade inflammation in the heart, and in turn, subcellular component abnormalities, such as oxidative stress, mitochondrial dysfunction, endoplasmic reticulum stress, and impaired calcium handling, leading to impaired myocardial relaxation. In the advanced stage, the vicious cycle of subcellular component abnormalities, inflammatory cell infiltration, and neurohumoral activation induces cardiomyocyte injury and death, and cardiac fibrosis, resulting in impairment of both diastolic and systolic functions. This review discusses some recent advances in understanding involvement of inflammation in metabolic cardiomyopathy.
Publisher: England
Language: English
Identifier: ISSN: 0008-6363
EISSN: 1755-3245
DOI: 10.1093/cvr/cvx012
PMID: 28395010
Source: GFMER Free Medical Journals
MEDLINE
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Inflammation and metabolic cardiomyopathy

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2017. For permissions, please email: journals.permissions@oup.com. ;ISSN: 0008-6363 ;EISSN: 1755-3245 ;DOI: 10.1093/cvr/cvx012 ;PMID: 28395010

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