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Molecular Insights into Skeletal Muscle Homeostasis and Metabolism

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Biochemistry, Molecular and Cellular Biology".

Deadline for manuscript submissions: closed (30 June 2024) | Viewed by 1878

Special Issue Editors


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Guest Editor
1. Victor Babes National Institute of Pathology, 050096 Bucharest, Romania
2. Faculty of Medicine, Carol Davila University of Medicine and Pharmacy, 050474 Bucharest, Romania
Interests: skeletal muscle; myogenesis; regeneration; cell culture; regenerative medicine
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
National Institute of Pathology “Victor Babes”, 050096 Bucharest, Romania
Interests: neuromuscular disorders; muscle regeneration; myokines; skeletal muscle; muscle biology; muscle damage; muscle proteins
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Homeostasis is the ability of muscular tissue to maintain a stable and constant internal environment and is essential for its proper functioning. This process plays a crucial role in health and requires maintaining a dynamic balance between muscle growth, repairing/regeneration as a response to injury stimuli, and tissue breakdown. Maintaining the cytoplasmic calcium homeostasis in skeletal muscle, for example, is very important for intracellular signaling activity and metabolism.

Metabolism plays a crucial role in maintaining a good and correct functioning of the skeletal muscle. It refers to the chemical processes occurring in cells to convert nutrients into energy and other essential molecules. The energy demands of skeletal muscle are high as it is the responsibility of physical movement, posture, regulation of body energy, and protein metabolism. Exercise and physical activity may have a significant impact on skeletal muscle metabolism, promoting energy expenditure and metabolic adaptations. More of this, maintaining a normal muscle mass helps in therapy involving pathological states of other organs, such as various forms of cancer with muscle cachexia, some neurodegenerative diseases, and others. The cross-talking between skeletal muscle and other tissues and organs involves the releasing of myokines which have anti-inflammatory, metabolic, and regenerative effects.

In pathological conditions, the homeostasis and metabolism of skeletal muscle are severely affected, and we believe that the papers in this Special Issue, addressing specific aspects of these processes, will help researchers to gather a better understanding of underlying mechanisms and signaling pathways, to highlight more appropriate therapeutic approaches to improve muscle physiology to counteract various myopathology and more.

Potential topics include, but are not limited to:

  • Niche satellite cells and cells communication in muscle homeostasis and metabolism dysregulations;
  • Myofiber regeneration/repair in different pathological conditions;
  • Muscle wasting disorders (myopathies, sarcopenia, cachexia, and others);
  • Skeletal muscle inflammatory response;
  • Exercise in skeletal muscle mass maintenance, role of myokines, and other aspects;
  • Cytoplasmic calcium homeostasis dysregulation, mitochondrion response, and endoplasmic reticulum stress.

We would also like to thank Dr. Gisela Gaina for her contribution and support for this special issue.

Dr. Laura Cristina Ceafalan
Dr. Emilia Manole
Guest Editors

Manuscript Submission Information

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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. Current Issues in Molecular 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 2200 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

  • skeletal muscle
  • muscle metabolism
  • rhabdomyolysis
  • storage diseases
  • neuromuscular weakness
  • mitochondrial myopathies
  • myofiber regeneration/repair

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Published Papers (1 paper)

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Research

10 pages, 3319 KiB  
Article
Presynaptic Purinergic Modulation of the Rat Neuro-Muscular Transmission
by Adel E. Khairullin, Sergey N. Grishin and Ayrat U. Ziganshin
Curr. Issues Mol. Biol. 2023, 45(10), 8492-8501; https://doi.org/10.3390/cimb45100535 - 19 Oct 2023
Cited by 2 | Viewed by 1367
Abstract
ATP, being a well-known universal high-energy compound, plays an important role as a signaling molecule and together with its metabolite adenosine they both attenuate the release of acetylcholine in the neuro-muscular synapse acting through membrane P2 and P1 receptors, respectively. In this work, [...] Read more.
ATP, being a well-known universal high-energy compound, plays an important role as a signaling molecule and together with its metabolite adenosine they both attenuate the release of acetylcholine in the neuro-muscular synapse acting through membrane P2 and P1 receptors, respectively. In this work, using a mechanomyographic method, we analyzed the presynaptic mechanisms by which ATP and adenosine can modulate the transduction in the rat m. soleus and m. extensor digitorum longus. N-ethylmaleimide, a G-protein antagonist, prevents the modulating effects of both ATP and adenosine. The action of ATP is abolished by chelerythrin, a specific phospholipase C inhibitor, while the inhibitory effect of adenosine is slightly increased by Rp-cAMPS, an inhibitor of protein kinase A, and by nitrendipine, a blocker of L-type Ca2+ channels. The addition of DPCPX, an A1 receptor antagonist, fully prevents the inhibitory action of adenosine in both muscles. Our data indicate that the inhibitory action of ATP involves metabotropic P2Y receptors and is mediated by phospholipase C dependent processes in rat motor neuron terminals. We suggest that the presynaptic effect of adenosine consists of negative and positive actions. The negative action occurs by stimulation of adenosine A1 receptors while the positive action is associated with the stimulation of adenosine A2A receptors, activation of protein kinase A and opening of L-type calcium channels. The combined mechanism of the modulating action of ATP and adenosine provides fine tuning of the synapse to fast changing conditions in the skeletal muscles. Full article
(This article belongs to the Special Issue Molecular Insights into Skeletal Muscle Homeostasis and Metabolism)
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