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Biology
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Role of Mitochondria in Muscle Disorders
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Role of Mitochondria in Muscle Disorders

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Cell Biology".

Deadline for manuscript submissions: closed (15 November 2023) | Viewed by 2215

Special Issue Editor

Prof. Dr. Steve Lancel

E-Mail Website
Guest Editor
Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1167-RID-AGE-Facteurs de Risque et Déterminants Moléculaires des Maladies Liées au Vieillissement, F-59000 Lille, France
Interests: mitochondria; endoplasmic reticulum; calcium; skeletal muscle; aging; inflammation; apoptosis; autophagy; receptor for advanced glycation end-products

Special Issue Information

Dear Colleagues,

Skeletal muscle is a specialized tissue that exerts several functions based on its contractile properties, such as locomotion, facial expression, posture, and breathing, but may also be considered as a key endocrine and metabolic organ. Its importance is revealed by many diseases, including myasthenia, myopathies, muscular dystrophies, rhabdomyolysis, and inflammatory muscle disorders. The proper function of skeletal muscle relies on a developed differentiation process that leads to sarcomeric organization and developed sarcoplasmic reticulum and mitochondria networks. Mitochondria are key organelles that, besides their well-known role in cellular energy production, represent an integrative signaling platform that controls cell fate.

This Special Issue will highlight new findings on how mitochondria modulate cellular pathways that may change skeletal muscle function in pathophysiological conditions.

Prof. Dr. Steve Lancel
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • mitochondria
  • skeletal muscle
  • signaling
  • metabolism
  • contraction

Published Papers (1 paper)

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Research

23 pages, 3235 KiB  
Article
Sepsis-like Energy Deficit Is Not Sufficient to Induce Early Muscle Fiber Atrophy and Mitochondrial Dysfunction in a Murine Sepsis Model
by Alexandre Pierre, Claire Bourel, Raphael Favory, Benoit Brassart, Frederic Wallet, Frederic N. Daussin, Sylvain Normandin, Michael Howsam, Raphael Romien, Jeremy Lemaire, Gaelle Grolaux, Arthur Durand, Marie Frimat, Bruno Bastide, Philippe Amouyel, Eric Boulanger, Sebastien Preau and Steve Lancel
Biology 2023, 12(4), 529; https://doi.org/10.3390/biology12040529 - 30 Mar 2023
Viewed by 1890
Abstract
Sepsis-induced myopathy is characterized by muscle fiber atrophy, mitochondrial dysfunction, and worsened outcomes. Whether whole-body energy deficit participates in the early alteration of skeletal muscle metabolism has never been investigated. Three groups were studied: “Sepsis” mice, fed ad libitum with a spontaneous decrease [...] Read more.
Sepsis-induced myopathy is characterized by muscle fiber atrophy, mitochondrial dysfunction, and worsened outcomes. Whether whole-body energy deficit participates in the early alteration of skeletal muscle metabolism has never been investigated. Three groups were studied: “Sepsis” mice, fed ad libitum with a spontaneous decrease in caloric intake (n = 17), and “Sham” mice fed ad libitum (Sham fed (SF), n = 13) or subjected to pair-feeding (Sham pair fed (SPF), n = 12). Sepsis was induced by the intraperitoneal injection of cecal slurry in resuscitated C57BL6/J mice. The feeding of the SPF mice was restricted according to the food intake of the Sepsis mice. Energy balance was evaluated by indirect calorimetry over 24 h. The tibialis anterior cross-sectional area (TA CSA), mitochondrial function (high-resolution respirometry), and mitochondrial quality control pathways (RTqPCR and Western blot) were assessed 24 h after sepsis induction. The energy balance was positive in the SF group and negative in both the SPF and Sepsis groups. The TA CSA did not differ between the SF and SPF groups, but was reduced by 17% in the Sepsis group compared with the SPF group (p < 0.05). The complex-I-linked respiration in permeabilized soleus fibers was higher in the SPF group than the SF group (p < 0.05) and lower in the Sepsis group than the SPF group (p < 0.01). Pgc1α protein expression increased 3.9-fold in the SPF mice compared with the SF mice (p < 0.05) and remained unchanged in the Sepsis mice compared with the SPF mice; the Pgc1α mRNA expression decreased in the Sepsis compared with the SPF mice (p < 0.05). Thus, the sepsis-like energy deficit did not explain the early sepsis-induced muscle fiber atrophy and mitochondrial dysfunction, but led to specific metabolic adaptations not observed in sepsis. Full article
(This article belongs to the Special Issue Role of Mitochondria in Muscle Disorders)
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