Abstract
Sarcopenia has been defined as a progressive decline of skeletal muscle mass, strength, and functions in elderly people. It is accompanied by physical frailty, functional disability, falls, hospitalization, and mortality, and is becoming a major geriatric disorder owing to the increasing life expectancy and growing older population worldwide. Experimental models are critical to understand the pathophysiology of sarcopenia and develop therapeutic strategies. Although its etiologies remain to be further elucidated, several mechanisms of sarcopenia have been identified, including cellular senescence, proteostasis imbalance, oxidative stress, and “inflammaging.” In this article, we address three main aspects. First, we describe the fundamental aging mechanisms. Next, we discuss both in vitro and in vivo experimental models based on molecular mechanisms that have the potential to elucidate the biochemical processes integral to sarcopenia. The use of appropriate models to reflect sarcopenia and/or its underlying pathways will enable researchers to understand sarcopenia and develop novel therapeutic strategies for sarcopenia. Lastly, we discuss the possible molecular targets and the current status of drug candidates for sarcopenia treatment. In conclusion, the development of experimental models for sarcopenia is essential to discover molecular targets that are valuable as biochemical biomarkers and/or therapeutic targets for sarcopenia.
Highlights
Three decades ago, sarcopenia was defined as a progressive decline of skeletal muscle mass, strength, and function [1]
The processes underlying sarcopenia development do include sarcopenic mechanisms and include indirect mechanisms related to the skeletal muscle environment
Compared with in vitro models, the use of animal models with natural aging or genetically modified animals offers the advantage of studying the systemic effects of sarcopenia, organ-level molecular patterns, and biochemical biomarkers
Summary
Three decades ago, sarcopenia was defined as a progressive decline of skeletal muscle mass, strength, and function [1]. It is widely accepted that aging is accompanied by the progressive decline of skeletal muscle mass, strength, and functions, which may be accelerated in some elderly people due to genetic, lifestyle, and environmental factors [3]. Cells 2020, 9, 1385 might be essential for sarcopenia prevention and defining the therapeutic strategies of new drug discovery. We discuss the fundamental aging mechanisms leading to sarcopenia, summarize the in vitro and in vivo experimental models used to define the molecular and cellular changes in skeletal muscle aging, and provide potential strategies for prevention and treatment of sarcopenia as well as approaches for further development of anti-sarcopenia therapeutics
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