scholarly journals Vitamin D Restores Skeletal Muscle Cell Remodeling and Myogenic Program: Potential Impact on Human Health

2021 ◽  
Vol 22 (4) ◽  
pp. 1760
Author(s):  
Clara Crescioli
Keyword(s):  
Skeletal Muscle ◽  
Vitamin D ◽  
Human Health ◽  
Muscle Cell ◽  
Vitamin D Insufficiency ◽  
Skeletal Muscle Cell ◽  
Tissue Integrity ◽  
Vitamin D Levels ◽  
Cell Remodeling ◽  
Myogenic Program

Skeletal muscle cells, albeit classified as vitamin D receptor (VDR)-poor cells, are finely controlled by vitamin D through genomic and non-genomic mechanisms. Skeletal muscle constantly undergoes cell remodeling, a complex system under multilevel regulation, mainly orchestrated by the satellite niche in response to a variety of stimuli. Cell remodeling is not limited to satisfy reparative and hypertrophic needs, but, through myocyte transcriptome/proteome renewal, it warrants the adaptations necessary to maintain tissue integrity. While vitamin D insufficiency promotes cell maladaptation, restoring vitamin D levels can correct/enhance the myogenic program. Hence, vitamin D fortified foods or supplementation potentially represents the desired approach to limit or avoid muscle wasting and ameliorate health. Nevertheless, consensus on protocols for vitamin D measurement and supplementation is still lacking, due to the high variability of lab tests and of the levels required in different contexts (i.e., age, sex, heath status, lifestyle). This review aims to describe how vitamin D can orchestrate skeletal muscle cell remodeling and myogenic programming, after reviewing the main processes and cell populations involved in this important process, whose correct progress highly impacts on human health. Topics on vitamin D optimal levels, supplementation and blood determination, which are still under debate, will be addressed.

scholarly journals Vitamin D Merging into Immune System-Skeletal Muscle Network: Effects on Human Health

2020 ◽  
Vol 10 (16) ◽  
pp. 5592
Author(s):  
Clara Crescioli
Keyword(s):  
Skeletal Muscle ◽  
Vitamin D ◽  
Immune System ◽  
Human Health ◽  
Hypovitaminosis D ◽  
Vitamin D Supplementation ◽  
Whole Body ◽  
Protective Effects ◽  
Skeletal Muscle Function ◽  
Vitamin D Levels

The concept that extra-skeletal functions of vitamin D impact on human health have taken place since quite ago. Among all, the beneficial effects of vitamin D on immune regulation, skeletal muscle function, and metabolism are undeniable. Adequate vitamin D levels maintain the immune system and skeletal muscle metabolism integrity, promoting whole-body homeostasis; hypovitaminosis D associates with the important decline of both tissues and promotes chronic inflammation, which is recognized to underlie several disease developments. Growing evidence shows that the immune system and skeletal muscle reciprocally dialogue, modulating each other’s function. Within this crosstalk, vitamin D seems able to integrate and converge some biomolecular signaling towards anti-inflammatory protective effects. Thus, vitamin D regulation appears even more critical at the immune system-muscle signaling intersection, rather than at the single tissue level, opening to wider/newer opportunities in clinical applications to improve health. This paper aims to focus on the immune system-skeletal muscle interplay as a multifaceted target for vitamin D in health and disease after recalling the main regulatory functions of vitamin D on those systems, separately. Some myokines, particularly relevant within the immune system/skeletal muscle/vitamin D networking, are discussed. Since vitamin D supplementation potentially offers the opportunity to maintain health, comments on this issue, still under debate, are included.

THE MYOGRAM OF THE ISOLATED SKELETAL MUSCLE CELL

Science ◽  
1930 ◽  
Vol 72 (1853) ◽  
pp. 17-18 ◽  
Author(s):  
D. E. S. Brown ◽  
F. J. M. Sichel
Keyword(s):  
Skeletal Muscle ◽  
Muscle Cell ◽  
Skeletal Muscle Cell

scholarly journals Human and rat skeletal muscle single-nuclei multi-omic integrative analyses nominate causal cell types, regulatory elements, and SNPs for complex traits

2021 ◽  
Author(s):  
Peter Orchard ◽  
Nandini Manickam ◽  
Christa Ventresca ◽  
Swarooparani Vadlamudi ◽  
Arushi Varshney ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Cell ◽  
Muscle Fiber ◽  
Cell Types ◽  
Chromatin Accessibility ◽  
Skeletal Muscle Cell ◽  
Rna Seq ◽  
Rat Skeletal Muscle ◽  
Integrative Analyses ◽  
Single Nucleus

Skeletal muscle accounts for the largest proportion of human body mass, on average, and is a key tissue in complex diseases and mobility. It is composed of several different cell and muscle fiber types. Here, we optimize single-nucleus ATAC-seq (snATAC-seq) to map skeletal muscle cell–specific chromatin accessibility landscapes in frozen human and rat samples, and single-nucleus RNA-seq (snRNA-seq) to map cell-specific transcriptomes in human. We additionally perform multi-omics profiling (gene expression and chromatin accessibility) on human and rat muscle samples. We capture type I and type II muscle fiber signatures, which are generally missed by existing single-cell RNA-seq methods. We perform cross-modality and cross-species integrative analyses on 33,862 nuclei and identify seven cell types ranging in abundance from 59.6% to 1.0% of all nuclei. We introduce a regression-based approach to infer cell types by comparing transcription start site–distal ATAC-seq peaks to reference enhancer maps and show consistency with RNA-based marker gene cell type assignments. We find heterogeneity in enrichment of genetic variants linked to complex phenotypes from the UK Biobank and diabetes genome-wide association studies in cell-specific ATAC-seq peaks, with the most striking enrichment patterns in muscle mesenchymal stem cells (∼3.5% of nuclei). Finally, we overlay these chromatin accessibility maps on GWAS data to nominate causal cell types, SNPs, transcription factor motifs, and target genes for type 2 diabetes signals. These chromatin accessibility profiles for human and rat skeletal muscle cell types are a useful resource for nominating causal GWAS SNPs and cell types.

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