The search for effective therapies to treat muscular dystrophies, particularly Duchenne muscular dystrophy (DMD), has been a persistent and formidable challenge. This research is motivated by the urgent need to address the complex pathophysiology of these debilitating diseases, which significantly compromise patients’ quality of life and lifespan.
DMD, in particular, poses a substantial challenge due to its progressive nature and severe impairment of skeletal muscle function. The genetic etiology of the disease, characterized by mutations in the dystrophin gene, initiates a cascade of pathological events, including chronic inflammation.
This Research Topic provides innovative therapeutic strategies targeting inflammation in muscular dystrophies, including the exploration of innate immunity, the therapeutic potential of growth hormone secretagogues, the underlying mechanisms of inflammation-induced muscle atrophy, and the regenerative capabilities of extracellular vesicle-derived miRNAs.
Petrof et al. present a compelling case for the involvement of trained immunity in the pathogenesis of DMD, emphasizing the role of dysregulated inflammation mediated by innate immune cells. Their findings establish a novel framework wherein epigenetic and metabolic alterations induce a hyper-responsive state in innate immune cells, potentially exacerbating tissue damage in DMD.
Complementing this perspective, Boccanegra et al. provide preclinical evidence supporting the therapeutic potential of growth hormone secretagogues (GHS) in DMD. GHSs have demonstrated efficacy in attenuating key drivers of disease progression such as inflammation and fibrosis, and concomitantly exhibited beneficial effects on muscle function and metabolism, suggesting a multifaceted therapeutic potential for improving the quality of life in DMD patients.
In parallel, Liu et al. explore the intricate relationship between inflammation and skeletal muscle atrophy, particularly in the context of sepsis-induced complications. Their investigation of the NLRP3 inflammasome reveals a critical role in driving catabolic processes, implicating it as a potential target for mitigating muscle wasting and associated comorbidities.
Finally, Yedigaryan et al. highlight the therapeutic potential of extracellular vesicle-derived miRNAs in muscle wasting conditions. Through a comprehensive analysis, they identify a hypertrophic miRNA signature capable of enhancing myogenic capacity and attenuating muscle degeneration. This promising approach holds significant implications to stimulate muscle repair and function.
In conclusion, the presented studies underscore the imperative for a multidisciplinary approach to address the challenges posed by DMD. The synergy between basic research, clinical studies, and drug development is essential for identifying novel therapeutic strategies and improving patient quality of life.
Statements
Author contributions
YT: Writing – review & editing. CV: Writing – original draft. AF: Writing – original draft.
Conflict of interest
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision.
Publisher’s note
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.
Summary
Keywords
miRNA, DMD, muscular dystrophies, inflammation, GHS (growth hormone secretagogues), NLRP3
Citation
Villa C, Farini A and Torrente Y (2024) Editorial: Inflammation in muscular dystrophies: mediators, mechanisms, and therapeutics. Front. Immunol. 15:1470266. doi: 10.3389/fimmu.2024.1470266
Received
25 July 2024
Accepted
12 August 2024
Published
22 August 2024
Volume
15 - 2024
Edited and reviewed by
Pietro Ghezzi, University of Urbino Carlo Bo, Italy
Updates
Copyright
© 2024 Villa, Farini and Torrente.
This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Yvan Torrente, yvan.torrente@unimi.it
Disclaimer
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.