<p>Sarcopenia is an age-related degenerative disease of skeletal muscles, characterized by progressively declined muscle mass, strength, and physical function. The prevalence of sarcopenia ranges from 11% to 50% among the global elderly population. The etiology of sarcopenia is multifactorial, including protein homeostasis imbalance, mitochondrial dysfunction, muscle satellite cells (MuSCs) dysfunction, chronic low-grade inflammation, and muscle interstitial remodeling. FAPs are mesenchymal-derived progenitor cells, playing crucial roles in maintaining muscle homeostasis and in the progression of sarcopenia. Under physiological conditions, FAPs interact with MuSCs and immune cells through their paracrine functions, providing supportive microenvironment for the growth and maintenance of muscle cells and MuSCs. Conversely, under pathological conditions, the abnormally activated and differentiated FAPs generated excessive intramuscular fat and fibrous tissue, which exacerbate the loss of muscle mass and strength in sarcopenia patients. The fate of FAPs are regulated by a complex signaling network composed by multiple pathways such as Wnt, Notch, and TGF-β/Smad, the dysregulation of which significantly contributes to the pathological differentiation of FAPs. Recently, single-cell sequencing technology have facilitated the identification of various FAP subpopulations, and provides new insights into the role of FAPs in sarcopenia. However, there are no specific therapeutic drugs for sarcopenia. Targeting molecules that govern FAP fate or eliminating dysfunctional FAP subpopulations represents a promising therapeutic strategy. Our review discusses the current understanding of sarcopenia and the role of FAPs in sarcopenia, and summarizes several novel therapeutic strategies targeting FAPs for the treatment of sarcopenia.</p>