Signaling via the Interleukin-10 Receptor Attenuates Cardiac Hypertrophy in Mice During Pressure Overload, but not Isoproterenol Infusion.

cardiac hypertrophy heart failure inflammation interleukin-10 signaling pathway

Journal

Frontiers in pharmacology
ISSN: 1663-9812
Titre abrégé: Front Pharmacol
Pays: Switzerland
ID NLM: 101548923

Informations de publication

Date de publication:
2020
Historique:
received: 05 05 2020
accepted: 06 10 2020
entrez: 16 11 2020
pubmed: 17 11 2020
medline: 17 11 2020
Statut: epublish

Résumé

Inflammation plays a key role during cardiac hypertrophy and the development of heart failure. Interleukin-10 (IL-10) is a major anti-inflammatory cytokine that is expressed in the heart and may play a crucial role in cardiac remodeling. Based on the evidence that IL-10 potentially reduces pathological hypertrophy, it was hypothesized that signaling via the IL-10 receptor (IL10R) in the heart produces a protective role in reducing cardiac hypertrophy. The aim of this study was to investigate the effects of the ablation of

Identifiants

pubmed: 33192505
doi: 10.3389/fphar.2020.559220
pii: 559220
pmc: PMC7662881
doi:

Types de publication

Journal Article

Langues

eng

Pagination

559220

Subventions

Organisme : British Heart Foundation
ID : PG/16/77/32400
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/P015816/1
Pays : United Kingdom
Organisme : British Heart Foundation
ID : PG/17/78/33304
Pays : United Kingdom
Organisme : British Heart Foundation
ID : PG/18/40/33767
Pays : United Kingdom
Organisme : British Heart Foundation
ID : PG/11/23/28801
Pays : United Kingdom
Organisme : Medical Research Council
ID : G1002082
Pays : United Kingdom

Informations de copyright

Copyright © 2020 Stafford, Assrafally, Prehar, Zi, De Morais, Maqsood, Cartwright, Muller and Oceandy.

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Auteurs

Nicholas Stafford (N)

Division of Cardiovascular Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, United Kingdom.
Manchester Academic Health Science Centre, The University of Manchester, Manchester, United Kingdom.

Farryah Assrafally (F)

Division of Cardiovascular Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, United Kingdom.
Manchester Academic Health Science Centre, The University of Manchester, Manchester, United Kingdom.

Sukhpal Prehar (S)

Division of Cardiovascular Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, United Kingdom.
Manchester Academic Health Science Centre, The University of Manchester, Manchester, United Kingdom.

Min Zi (M)

Division of Cardiovascular Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, United Kingdom.
Manchester Academic Health Science Centre, The University of Manchester, Manchester, United Kingdom.

Ana M De Morais (AM)

Division of Cardiovascular Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, United Kingdom.
Manchester Academic Health Science Centre, The University of Manchester, Manchester, United Kingdom.

Arfa Maqsood (A)

Division of Cardiovascular Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, United Kingdom.
Manchester Academic Health Science Centre, The University of Manchester, Manchester, United Kingdom.

Elizabeth J Cartwright (EJ)

Division of Cardiovascular Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, United Kingdom.
Manchester Academic Health Science Centre, The University of Manchester, Manchester, United Kingdom.

Werner Mueller (W)

School of Biological Sciences, The University of Manchester, Manchester, United Kingdom.

Delvac Oceandy (D)

Division of Cardiovascular Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, United Kingdom.
Manchester Academic Health Science Centre, The University of Manchester, Manchester, United Kingdom.

Classifications MeSH