Mediators and Patterns of Muscle Loss in Chronic Systemic Inflammation

Besides its primary function in locomotion, skeletal muscle (SKM), which represents up to half of human's weight, also plays a fundamental homeostatic role. Through the secretion of soluble peptides, or myokines, SKM interacts with major organs involved in metabolic processes. In turn, metaboli...

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Main Authors: Sandra Pérez-Baos, Iván Prieto-Potin, Jorge A. Román-Blas, Olga Sánchez-Pernaute, Raquel Largo, Gabriel Herrero-Beaumont
Format: Article
Language:English
Published: Frontiers Media S.A. 2018-04-01
Series:Frontiers in Physiology
Subjects:
Online Access:http://journal.frontiersin.org/article/10.3389/fphys.2018.00409/full
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author Sandra Pérez-Baos
Iván Prieto-Potin
Jorge A. Román-Blas
Olga Sánchez-Pernaute
Raquel Largo
Gabriel Herrero-Beaumont
author_facet Sandra Pérez-Baos
Iván Prieto-Potin
Jorge A. Román-Blas
Olga Sánchez-Pernaute
Raquel Largo
Gabriel Herrero-Beaumont
author_sort Sandra Pérez-Baos
collection DOAJ
description Besides its primary function in locomotion, skeletal muscle (SKM), which represents up to half of human's weight, also plays a fundamental homeostatic role. Through the secretion of soluble peptides, or myokines, SKM interacts with major organs involved in metabolic processes. In turn, metabolic cues from these organs are received by muscle cells, which adapt their response accordingly. This is done through an intricate intracellular signaling network characterized by the cross-talking between anabolic and catabolic pathways. A fine regulation of the network is required to protect the organism from an excessive energy expenditure. Systemic inflammation evokes a catabolic reaction in SKM known as sarcopenia. In turn this response comprises several mechanisms, which vary depending on the nature of the insult and its magnitude. In this regard, aging, chronic inflammatory systemic diseases, osteoarthritis and idiopathic inflammatory myopathies can lead to muscle loss. Interestingly, sarcopenia may persist despite remission of chronic inflammation, an issue which warrants further research. The Janus kinase/signal transducer and activator of transcription (JAK/STAT) system stands as a major participant in muscle loss during systemic inflammation, while it is also a well-recognized orchestrator of muscle cell turnover. Herein we summarize current knowledge about models of sarcopenia, their triggers and major mediators and their effect on both protein and cell growth yields. Also, the dual action of the JAK/STAT pathway in muscle mass changes is discussed. We highlight the need to unravel the precise contribution of this system to sarcopenia in order to design targeted therapeutic strategies.
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spelling doaj.art-ac9faf1497e84af799d8d6e63266dc242022-12-22T03:30:05ZengFrontiers Media S.A.Frontiers in Physiology1664-042X2018-04-01910.3389/fphys.2018.00409343676Mediators and Patterns of Muscle Loss in Chronic Systemic InflammationSandra Pérez-BaosIván Prieto-PotinJorge A. Román-BlasOlga Sánchez-PernauteRaquel LargoGabriel Herrero-BeaumontBesides its primary function in locomotion, skeletal muscle (SKM), which represents up to half of human's weight, also plays a fundamental homeostatic role. Through the secretion of soluble peptides, or myokines, SKM interacts with major organs involved in metabolic processes. In turn, metabolic cues from these organs are received by muscle cells, which adapt their response accordingly. This is done through an intricate intracellular signaling network characterized by the cross-talking between anabolic and catabolic pathways. A fine regulation of the network is required to protect the organism from an excessive energy expenditure. Systemic inflammation evokes a catabolic reaction in SKM known as sarcopenia. In turn this response comprises several mechanisms, which vary depending on the nature of the insult and its magnitude. In this regard, aging, chronic inflammatory systemic diseases, osteoarthritis and idiopathic inflammatory myopathies can lead to muscle loss. Interestingly, sarcopenia may persist despite remission of chronic inflammation, an issue which warrants further research. The Janus kinase/signal transducer and activator of transcription (JAK/STAT) system stands as a major participant in muscle loss during systemic inflammation, while it is also a well-recognized orchestrator of muscle cell turnover. Herein we summarize current knowledge about models of sarcopenia, their triggers and major mediators and their effect on both protein and cell growth yields. Also, the dual action of the JAK/STAT pathway in muscle mass changes is discussed. We highlight the need to unravel the precise contribution of this system to sarcopenia in order to design targeted therapeutic strategies.http://journal.frontiersin.org/article/10.3389/fphys.2018.00409/fullskeletal muscleturnoveranabolismcatabolismsarcopeniamyokines
spellingShingle Sandra Pérez-Baos
Iván Prieto-Potin
Jorge A. Román-Blas
Olga Sánchez-Pernaute
Raquel Largo
Gabriel Herrero-Beaumont
Mediators and Patterns of Muscle Loss in Chronic Systemic Inflammation
Frontiers in Physiology
skeletal muscle
turnover
anabolism
catabolism
sarcopenia
myokines
title Mediators and Patterns of Muscle Loss in Chronic Systemic Inflammation
title_full Mediators and Patterns of Muscle Loss in Chronic Systemic Inflammation
title_fullStr Mediators and Patterns of Muscle Loss in Chronic Systemic Inflammation
title_full_unstemmed Mediators and Patterns of Muscle Loss in Chronic Systemic Inflammation
title_short Mediators and Patterns of Muscle Loss in Chronic Systemic Inflammation
title_sort mediators and patterns of muscle loss in chronic systemic inflammation
topic skeletal muscle
turnover
anabolism
catabolism
sarcopenia
myokines
url http://journal.frontiersin.org/article/10.3389/fphys.2018.00409/full
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