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Molecular and phenotypic analysis of rodent models reveals conserved and species-specific modulators of human sarcopenia
JournalArticle (Originalarbeit in einer wissenschaftlichen Zeitschrift)
 
ID 4616664
Author(s) Börsch, Anastasiya; Ham, Daniel J.; Mittal, Nitish; Tintignac, Lionel A.; Migliavacca, Eugenia; Feige, Jérôme N.; Rüegg, Markus A.; Zavolan, Mihaela
Author(s) at UniBasel Zavolan, Mihaela
Börsch, Anastasiya
Ham, Daniel Jacob
Mittal, Nitish
Tintignac, Lionel
Rüegg, Markus A.
Year 2021
Title Molecular and phenotypic analysis of rodent models reveals conserved and species-specific modulators of human sarcopenia
Journal Communications Biology
Volume 4
Number 1
Pages / Article-Number 194
Mesh terms Age Factors; Aging, pathology; Animals; Body Composition; Disease Models, Animal; Disease Progression; Gene Expression Regulation; Humans; Male; Mice, Inbred C57BL; Muscle, Skeletal, physiopathology; Phenotype; Rats; Sarcopenia, physiopathology; Signal Transduction; Species Specificity; Transcriptome
Abstract Sarcopenia, the age-related loss of skeletal muscle mass and function, affects 5-13% of individuals aged over 60 years. While rodents are widely-used model organisms, which aspects of sarcopenia are recapitulated in different animal models is unknown. Here we generated a time series of phenotypic measurements and RNA sequencing data in mouse gastrocnemius muscle and analyzed them alongside analogous data from rats and humans. We found that rodents recapitulate mitochondrial changes observed in human sarcopenia, while inflammatory responses are conserved at pathway but not gene level. Perturbations in the extracellular matrix are shared by rats, while mice recapitulate changes in RNA processing and autophagy. We inferred transcription regulators of early and late transcriptome changes, which could be targeted therapeutically. Our study demonstrates that phenotypic measurements, such as muscle mass, are better indicators of muscle health than chronological age and should be considered when analyzing aging-related molecular data.
Publisher Springer Nature
ISSN/ISBN 2399-3642
edoc-URL https://edoc.unibas.ch/82028/
Full Text on edoc No
Digital Object Identifier DOI 10.1038/s42003-021-01723-z
PubMed ID http://www.ncbi.nlm.nih.gov/pubmed/33580198
ISI-Number WOS:000620242500001
Document type (ISI) Journal Article
 
   

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