PUBLICATION
Zebrafish models of sarcopenia
- Authors
- Daya, A., Donaka, R., Karasik, D.
- ID
- ZDB-PUB-200422-140
- Date
- 2020
- Source
- Disease models & mechanisms 13(3): (Review)
- Registered Authors
- Daya, Alon
- Keywords
- Aging, GWAS, Genome, Imaging, Muscle disease, Sarcopenia, Zebrafish
- MeSH Terms
-
- Animals
- Biomedical Research
- Disease Models, Animal*
- Genome-Wide Association Study
- Muscle, Skeletal/pathology
- Sarcopenia/diagnosis
- Sarcopenia/genetics
- Sarcopenia/pathology*
- Zebrafish/genetics
- Zebrafish/physiology*
- PubMed
- 32298234 Full text @ Dis. Model. Mech.
Citation
Daya, A., Donaka, R., Karasik, D. (2020) Zebrafish models of sarcopenia. Disease models & mechanisms. 13(3):.
Abstract
Sarcopenia - the accelerated age-related loss of muscle mass and function - is an under-diagnosed condition, and is central to deteriorating mobility, disability and frailty in older age. There is a lack of treatment options for older adults at risk of sarcopenia. Although sarcopenia's pathogenesis is multifactorial, its major phenotypes - muscle mass and muscle strength - are highly heritable. Several genome-wide association studies of muscle-related traits were published recently, providing dozens of candidate genes, many with unknown function. Therefore, animal models are required not only to identify causal mechanisms, but also to clarify the underlying biology and translate this knowledge into new interventions. Over the past several decades, small teleost fishes had emerged as powerful systems for modeling the genetics of human diseases. Owing to their amenability to rapid genetic intervention and the large number of conserved genetic and physiological features, small teleosts - such as zebrafish, medaka and killifish - have become indispensable for skeletal muscle genomic studies. The goal of this Review is to summarize evidence supporting the utility of small fish models for accelerating our understanding of human skeletal muscle in health and disease. We do this by providing a basic foundation of the (zebra)fish skeletal muscle morphology and physiology, and evidence of muscle-related gene homology. We also outline challenges in interpreting zebrafish mutant phenotypes and in translating them to human disease. Finally, we conclude with recommendations on future directions to leverage the large body of tools developed in small fish for the needs of genomic exploration in sarcopenia.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping