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Ion Channels and Pumps in Skeletal Muscle

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (15 April 2024) | Viewed by 4194

Special Issue Editors


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Guest Editor
Inštitut za Patološko Fiziologijo, Univerze v Ljubljani Medicinske Fakultete, SI-1000 Ljubljana, Slovenia
Interests: AMPK; Na+,K+-ATPase; FXYD; skeletal muscle; myokines; neuro-muscular junction

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Guest Editor
Department of Life Sciences, University of Trieste, 34127 Trieste, Italy
Interests: ion channels; nAChR, neuro-muscular junction; intracellular Ca2+ homeostasis

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Guest Editor
Section of Integrative Physiology, Department of Molecular Medicine and Surgery, Karolinska Institutet, SE-171 77 Stockholm, Sweden
Interests: Na,K-ATPase; FXYD proteins; GLUT4; potassium homeostasis; type 2 diabetes

Special Issue Information

Dear Colleagues,

We would like to invite you to participate in a special issue of the International Journal of Molecular Sciences entitled Ion channels and pumps in skeletal muscle.

With more than 600 individual organs, which represent approximately 40% of the total body weight, skeletal muscles, when considered together, constitute the largest organ in the human body. As well as a contractile organ, which enables locomotion, posture, and breathing, skeletal muscles are a key metabolic organ, fundamentally important for the maintenance of systemic metabolic homeostasis, and an endocrine organ, which secretes hundreds of myokines that drive various adaptations in skeletal muscle and many other organs and organ systems, including immune system.

Skeletal muscles are also a major site of transmembrane and intracellular ion transport, which plays essential roles not only in muscle excitability and contractility, but also transmembrane transport of nutrients and intracellular signaling. Furthermore, being the largest store of K+ ions in the body, skeletal muscles buffer fluctuations in extracellular K+ concentrations, thus helping to prevent potentially dangerous hyperkalemia and hypokalemia. Not surprisingly, ion transporters, such as Na+,K+-ATPase and sarcoplasmic/endoplasmic reticulum calcium ATPase (SERCA), impose a significant energetic cost on skeletal muscle, which requires tight coordination between regulation of ion transport and energy metabolism in skeletal muscle. Finally, recent advances concerning biology of mechanosensitive cation channels, such as PIEZO, have highlighted novel potential mechanisms by which mechanical forces, such as during contractions, might modulate skeletal muscle function, thus adding a further layer of complexity to regulation of ion transport and its functional consequences in skeletal muscle.

Manuscripts that address ion channels and pumps in skeletal muscle under physiological and pathophysiological conditions and/or ion channels and pumps in skeletal muscle as pharmacological targets, including original research, methodological studies, reviews, as well as theoretical studies, which offer new insights into the understanding of experimental results or suggest new experimentally testable hypotheses, will be taken into consideration. The scope of the call includes, but is not limited to:

  • The role of on ion channels and pumps in skeletal muscle in health and disease.
  • The importance of ion transport in skeletal muscle for maintenance of systemic ion and energy homeostasis.
  • Regulation of ion channels and pumps in skeletal muscle.
  • The role of ion transport in skeletal muscle in secretion of myokines.
  • Experimental models, including cell cultures and isolated organs, for investigation of ion transport in skeletal muscle.
  • Effect of physical (in)activity on the ion transport in skeletal muscle.
  • Effects of ageing on the ion transport in skeletal muscle.
  • Cross-talk between ion transport and energy metabolism in skeletal muscle.
  • Energetics of ion transport in skeletal muscle.
  • Dysfunction of ion transport in skeletal muscle in the context of metabolic disorders, including insulin resistance and type 2 diabetes.
  • Pharmacological modulation of ion transport in skeletal muscle: ion channels and pumps as pharmacological targets.
  • The role of skeletal muscle innervation and effects of denervation on ion channels and pumps in skeletal muscle.
  • Ion channels and pumps in the context of sarcopenia: dysfunction of ion transport as the cause and consequence of muscle weakness and wasting.

Dr. Sergej Pirkmajer
Prof. Dr. Paola Lorenzon
Dr. Alexander V. Chibalin
Guest Editors

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • ion channels
  • Na+,K+-ATPase
  • FXYD
  • SERCA
  • PIEZO
  • myokines
  • energy metabolism
  • AMPK
  • exercise
  • physical inactivity
  • muscle wasting

Published Papers (2 papers)

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Research

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11 pages, 4745 KiB  
Article
A Pharmacological Investigation of the TMEM16A Currents in Murine Skeletal Myogenic Precursor Cells
by Marina Sciancalepore, Asja Ragnini, Paola Zacchi, Violetta Borelli, Paola D’Andrea, Paola Lorenzon and Annalisa Bernareggi
Int. J. Mol. Sci. 2024, 25(4), 2225; https://doi.org/10.3390/ijms25042225 - 13 Feb 2024
Viewed by 571
Abstract
TMEM16A is a Ca2+-activated Cl channel expressed in various species and tissues. In mammalian skeletal muscle precursors, the activity of these channels is still poorly investigated. Here, we characterized TMEM16A channels and investigated if the pharmacological activation of Piezo1 channels [...] Read more.
TMEM16A is a Ca2+-activated Cl channel expressed in various species and tissues. In mammalian skeletal muscle precursors, the activity of these channels is still poorly investigated. Here, we characterized TMEM16A channels and investigated if the pharmacological activation of Piezo1 channels could modulate the TMEM16A currents in mouse myogenic precursors. Whole-cell patch-clamp recordings combined with the pharmacological agents Ani9, T16inh-A01 and Yoda1 were used to characterize TMEM16A-mediated currents and the possible modulatory effect of Piezo1 activity on TMEM16A channels. Western blot analysis was also carried out to confirm the expression of TMEM16A and Piezo1 channel proteins. We found that TMEM16A channels were functionally expressed in fusion-competent mouse myogenic precursors. The pharmacological blockage of TMEM16A inhibited myocyte fusion into myotubes. Moreover, the specific Piezo1 agonist Yoda1 positively regulated TMEM16A currents. The findings demonstrate, for the first time, a sarcolemmal TMEM16A channel activity and its involvement at the early stage of mammalian skeletal muscle differentiation. In addition, the results suggest a possible role of mechanosensitive Piezo1 channels in the modulation of TMEM16A currents. Full article
(This article belongs to the Special Issue Ion Channels and Pumps in Skeletal Muscle)
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Review

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26 pages, 1830 KiB  
Review
Ion Channels of the Sarcolemma and Intracellular Organelles in Duchenne Muscular Dystrophy: A Role in the Dysregulation of Ion Homeostasis and a Possible Target for Therapy
by Mikhail V. Dubinin and Konstantin N. Belosludtsev
Int. J. Mol. Sci. 2023, 24(3), 2229; https://doi.org/10.3390/ijms24032229 - 23 Jan 2023
Cited by 9 | Viewed by 3040
Abstract
Duchenne muscular dystrophy (DMD) is caused by the absence of the dystrophin protein and a properly functioning dystrophin-associated protein complex (DAPC) in muscle cells. DAPC components act as molecular scaffolds coordinating the assembly of various signaling molecules including ion channels. DMD shows a [...] Read more.
Duchenne muscular dystrophy (DMD) is caused by the absence of the dystrophin protein and a properly functioning dystrophin-associated protein complex (DAPC) in muscle cells. DAPC components act as molecular scaffolds coordinating the assembly of various signaling molecules including ion channels. DMD shows a significant change in the functioning of the ion channels of the sarcolemma and intracellular organelles and, above all, the sarcoplasmic reticulum and mitochondria regulating ion homeostasis, which is necessary for the correct excitation and relaxation of muscles. This review is devoted to the analysis of current data on changes in the structure, functioning, and regulation of the activity of ion channels in striated muscles in DMD and their contribution to the disruption of muscle function and the development of pathology. We note the prospects of therapy based on targeting the channels of the sarcolemma and organelles for the correction and alleviation of pathology, and the problems that arise in the interpretation of data obtained on model dystrophin-deficient objects. Full article
(This article belongs to the Special Issue Ion Channels and Pumps in Skeletal Muscle)
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