International Journal of Molecular Sciences

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Research on Skeletal and Cardiac Muscle Regeneration Mechanisms

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Dear Colleagues,

The myogenic and cardiomyogenic differentiations of mesenchymal or other types of stem cells in vitro and in vivo are complex processes, which include cell responsiveness to various compounds and model systems, and direct or indirect interaction between cells and extracellular components, that further regulates intracellular signalling systems and tissue functioning. Despite their diversity, the regeneration mechanisms of skeletal and cardiac muscle occur within the striated muscle environment, whose primary goal is in vitro targeted regulation and subsequent in vivo translation, thereby allowing to improve muscle functioning.

In order to better understand the myogenic and cardiomyogenic differentiation processes and their regulation, both in vivo and in vitro myogenic model systems are of crucial importance. Therefore, this Special Issue aims to collate papers focusing on in vivo and in vitro myogenic and cardiomyogenic differentiation mechanisms that highlight new external or internal inductors, cell types, ECM components, scaffolds and other biomodulators to improve the regeneration of skeletal and cardiac muscles and expand their further clinical applications.

Dr. Daiva Bironaité
Guest Editor

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17 pages, 2992 KiB

Open AccessArticle

Class I and II Histone Deacetylase Inhibitors as Therapeutic Modulators of Dilated Cardiac Tissue-Derived Mesenchymal Stem/Stromal Cells

by Rokas Mikšiūnas, Siegfried Labeit and Daiva Bironaite

Int. J. Mol. Sci. 2024, 25(12), 6758; https://doi.org/10.3390/ijms25126758 - 19 Jun 2024

Viewed by 383

Abstract

The prevalence of dilated cardiomyopathy (DCM) is increasing globally, highlighting the need for innovative therapeutic approaches to prevent its onset. In this study, we examined the energetic and epigenetic distinctions between dilated and non-dilated human myocardium-derived mesenchymal stem/stromal cells (hmMSCs) and assessed the effects of class I and II HDAC inhibitors (HDACi) on these cells and their cardiomyogenic differentiation. Cells were isolated from myocardium biopsies using explant outgrowth methods. Mitochondrial and histone deacetylase activities, ATP levels, cardiac transcription factors, and structural proteins were assessed using flow cytometry, PCR, chemiluminescence, Western blotting, and immunohistochemistry. The data suggest that the tested HDAC inhibitors improved acetylation and enhanced the energetic status of both types of cells, with significant effects observed in dilated myocardium-derived hmMSCs. Additionally, the HDAC inhibitors activated the cardiac transcription factors Nkx2-5, HOPX, GATA4, and Mef2C, and upregulated structural proteins such as cardiac troponin T and alpha cardiac actin at both the protein and gene levels. In conclusion, our findings suggest that HDACi may serve as potential modulators of the energetic status and cardiomyogenic differentiation of human heart hmMSCs. This avenue of exploration could broaden the search for novel therapeutic interventions for dilated cardiomyopathy, ultimately leading to improvements in heart function. Full article

(This article belongs to the Special Issue Research on Skeletal and Cardiac Muscle Regeneration Mechanisms)

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15 pages, 4833 KiB

Open AccessArticle

The Transcription Factor Mohawk Facilitates Skeletal Muscle Repair via Modulation of the Inflammatory Environment

by Cherie Alissa Lynch, Sofia A. Acosta, Douglas M. Anderson, Gavin E. Rogers, Jeanne Wilson-Rawls and Alan Rawls

Int. J. Mol. Sci. 2024, 25(9), 5019; https://doi.org/10.3390/ijms25095019 - 4 May 2024

Viewed by 815

Abstract

Efficient repair of skeletal muscle relies upon the precise coordination of cells between the satellite cell niche and innate immune cells that are recruited to the site of injury. The expression of pro-inflammatory cytokines and chemokines such as TNFα, IFNγ, CXCL1, and CCL2, by muscle and tissue resident immune cells recruits neutrophils and M1 macrophages to the injury and activates satellite cells. These signal cascades lead to highly integrated temporal and spatial control of muscle repair. Despite the therapeutic potential of these factors for improving tissue regeneration after traumatic and chronic injuries, their transcriptional regulation is not well understood. The transcription factor Mohawk (Mkx) functions as a repressor of myogenic differentiation and regulates fiber type specification. Embryonically, Mkx is expressed in all progenitor cells of the musculoskeletal system and is expressed in human and mouse myeloid lineage cells. An analysis of mice deficient for Mkx revealed a delay in postnatal muscle repair characterized by impaired clearance of necrotic fibers and smaller newly regenerated fibers. Further, there was a delay in the expression of inflammatory signals such as Ccl2, Ifnγ, and Tgfß. This was coupled with impaired recruitment of pro-inflammatory macrophages to the site of muscle damage. These studies demonstrate that Mkx plays a critical role in adult skeletal muscle repair that is mediated through the initial activation of the inflammatory response. Full article

(This article belongs to the Special Issue Research on Skeletal and Cardiac Muscle Regeneration Mechanisms)

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