Myokines in Health and Diseases

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 10 September 2026 | Viewed by 315

Editors


E-Mail Website
Guest Editor
Department of Sport Exercise and Rehabilitation, Northumbria University, Newcastle-upon-Tyne NE1 8ST, UK
Interests: COPD; asthma; sarcopenia; osteopontin; extracellular matrix
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor Assistant
Department of Human Physiology and Pathophysiology, School of Medicine, Collegium Medicum, University of Warmia and Mazury in Olsztyn, 10-719 Olsztyn, Poland
Interests: clinical rheumatology; adult rheumatology; physiology; lung diseases; spirometry; respiratory physiology; pulmonary sarcoidosis; lung; interstitial lung disease; obstructive lung diseases; telemedicine; primary practice; COVID-19 pandemic

Special Issue Information

Dear Colleagues,

Myokines are signaling cytokines produced and released by skeletal muscle cells. They exert pleiotropic actions by interacting with specific receptors expressed in multiple organs. Their secretion is strongly stimulated by physical activity, through which myokines influence key biological processes, including metabolism, intracellular signaling cascades, and gene and protein expression, as well as cellular growth and differentiation. In terms of health, myokines such as irisin, myostatin, and brain-derived neurotrophic factor (BDNF) mediate many of the favorable adaptations induced by regular exercise. These include improved insulin responsiveness, more efficient lipid metabolism, enhanced cardiovascular performance, and protective effects on the nervous system. Conversely, alterations in myokine release or disruptions in their signaling pathways have been linked to the development of lifestyle-related disorders, such as obesity, type 2 diabetes mellitus, sarcopenia, osteoporosis, and cardiovascular diseases. Clarifying the mechanisms underlying myokine activity provides important insight into the molecular connections between physical activity, overall health, and disease prevention. Furthermore, myokines are increasingly being recognized as valuable biomarkers and as potential targets for therapeutic strategies aimed at treating metabolic and inflammatory conditions. We welcome the submission of both original research articles and comprehensive review papers.

Dr. Davina C. M. Simoes
Guest Editor

Dr. Lukasz Jaskiewicz
Guest Editor Assistant

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 communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly 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

  • myokines
  • skeletal muscle
  • metabolic regulation
  • chronic diseases
  • muscle–organ crosstalk

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Review

32 pages, 3567 KB  
Review
The Myokine Adaptome in Health and Disease: Exercise-Induced Cellular Signaling, Muscle–Organ Crosstalk, and Therapeutic Plasticity
by Dan Cristian Mănescu, Camelia Daniela Plastoi, Ancuța Pîrvan, Rodica Dîrnu, Elena Ancuța Floroiu and Andreea Popescu
Cells 2026, 15(14), 1236; https://doi.org/10.3390/cells15141236 - 9 Jul 2026
Abstract
Skeletal muscle is increasingly recognized as a dynamic secretory organ capable of translating contractile, metabolic, mechanical and inflammatory stimuli into systemic biological signals. Among these signals, myokines and myokine-associated exerkines mediate communication between skeletal muscle and distant organs, influencing glucose and lipid metabolism, [...] Read more.
Skeletal muscle is increasingly recognized as a dynamic secretory organ capable of translating contractile, metabolic, mechanical and inflammatory stimuli into systemic biological signals. Among these signals, myokines and myokine-associated exerkines mediate communication between skeletal muscle and distant organs, influencing glucose and lipid metabolism, immune regulation, bone remodeling, neuroplasticity, vascular function and tissue regeneration. Representative mediators considered include IL-6, IL-15, myostatin, follistatin, decorin, FNDC5/irisin, FGF21, myonectin/CTRP15, BDNF, cathepsin B, SPARC, apelin and extracellular-vesicle cargo. However, current evidence remains fragmented across individual molecules, exercise modalities, sampling windows, assay platforms and disease contexts. This narrative mechanistic review proposes the concept of the “myokine adaptome” as an integrated, context-dependent signaling network through which skeletal muscle contributes to systemic homeostasis in health and disease. We synthesize evidence on cellular triggers of myokine release, including AMPK-PGC-1α signaling, mTORC1-dependent mechanical sensing, calcium flux, redox signaling, inflammatory pathways and extracellular-vesicle-mediated communication. We further examine how exercise modality, aging, obesity, type 2 diabetes, sarcopenia, osteoporosis, cardiovascular disease, COPD, cancer/cachexia and chronic inflammation reshape myokine production and target-organ responsiveness. The central argument is that myokine biology should be interpreted not as a catalog of isolated mediators, but as a dynamic adaptive code defined by signal amplitude, temporal pattern, molecular composition, delivery route and recipient-tissue sensitivity. Its novelty is operational rather than nominal: it requires source confidence, temporal kinetics, co-signal context, delivery route and functional decoding to be evaluated together. This framework may improve biomarker design, disease-specific exercise prescription and therapeutic strategies aimed at restoring adaptive muscle–organ communication. The framework is further strengthened by testable predictions concerning adaptive pulsatility, modality-specific signatures, source attribution, recovery quality, disease-specific decoding and the superiority of multi-marker panels over single-molecule readouts. Full article
(This article belongs to the Special Issue Myokines in Health and Diseases)
Show Figures

Figure 1

Back to TopTop