Animal models of sarcopenia

• Type of Material: Article
• Authors: Courtney J. Christian, Emory University; Guy Benian, Emory University
• Language: English
• Date: 2020-08-28
• Publisher: WILEY
• Publication Version: Final Published Version
• Copyright Statement: © 2020 The Authors. Aging Cell published by Anatomical Society and John Wiley & Sons Ltd
• License: Creative Commons Attribution 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.1111/acel.13223
• Title of Journal or Parent Work: AGING CELL
• Volume: 19
• Issue: 10
• Start Page: e13223
• End Page: e13223
• Grant/Funding Information: This work was supported in part from NIH grant R01 GM118534 to A.F. Oberhauser and G.M. Benian, and a grant from the University Research Committee of Emory University to G.M.B.
• Keywords: rats; Life Sciences & Biomedicine; Cell Biology; AGE-RELATED-CHANGES; ZEBRAFISH DANIO-RERIO; EXERCISE; mice; MITOCHONDRIAL-FUNCTION; DIETARY RESTRICTION; Science & Technology; muscle; SKELETAL-MUSCLE; aging; zebrafish; DROSOPHILA; C-ELEGANS; INCREASES MUSCLE MASS; sarcopenia; Geriatrics & Gerontology; LIFE-SPAN; Caenorhabditis elegans; Drosophila
• Research Categories: Biology, Cell; Health Sciences, Nutrition; Gerontology

Abstract

Sarcopenia is the age-related decline in muscle mass and function without any underlying disease. The exact molecular mechanisms responsible for this pathology remain unknown. The use of model organisms, such as mice, rats, flies, and worms, has advanced the field of sarcopenia research by identifying therapeutic strategies and genetic mutations that result in improved muscle mass and function of elderly animals. This review discusses molecular and therapeutic discoveries made using these model organisms and how these animals can be further utilized to better understand sarcopenia pathogenesis. In rodents, flies, and worms, dietary restriction improves muscle performance in old animals. In rodents and worms, exercise and a number of naturally occurring compounds alleviate sarcopenia. Reduction in the insulin/IGF1 receptor pathway, well known to promote longevity, improves sarcopenia in worms and flies. Mitochondrial dysfunction may contribute to the pathogenesis of sarcopenia: In rodents, there is age-dependent reduction in mitochondrial mass and a change in morphology; in nematodes, there is age-dependent fragmentation of mitochondria that precedes sarcomeric disorganization. In Drosophila and rats, components of the 26S proteasome are elevated in aged muscle. An advantage of the worm and fly models is that these organisms lack muscle stem cells, and thus processes that promote the maintenance of already assembled muscle, can be identified without the confounding influence of muscle regeneration. Zebrafish are an up and coming model of sarcopenia for future consideration. A better understanding of the molecular changes behind sarcopenia will help researchers develop better therapies to improve the muscle health of elderly individuals.