Sarcopenia is an age-related progressive muscle degeneration condition characterized by loss of muscle mass, muscle strength, and poor physical function. Its prevalence and mortality rates continue to rise with advancing age, significantly impairing patients' quality of life. The pathogenesis of sarcopenia involves multiple pathophysiological processes, including imbalanced protein catabolism, cell death, mitochondrial dysfunction, and various cellular signaling pathways. Therefore, it is crucial to identify potential therapeutic targets and treatments for sarcopenia. As an exercise-induced myokine, irisin has shown great potential in maintaining skeletal muscle health. In this review, we focus on the relationship between irisin and sarcopenia, delving into existing research to elucidate irisin's mechanisms of action in sarcopenia—including its effects on protein catabolism, cell death, mitochondrial dysfunction, cellular signaling, and muscle cell proliferation and differentiation. We provide insights into irisin as a therapeutic intervention for sarcopenia and provide essential evidence to support its clinical application in sarcopenia treatment.

Osteosarcoma is an aggressive malignant neoplasm, and it is of great significance to the fabrication and investigation of the anti-tumor mechanism of nanomedicine in the treatment of osteosarcoma. Herein, a cinnamaldehyde polymeric prodrug micelle with pH-sensitive charge-conversion ability (mPEG-b-P(C7-co-CA)) was fabricated, and the anti-osteosarcoma mechanism of mPEG-b-P(C7-co-CA) micelle was investigated. mPEG-b-P(C7-co-CA) micelles were prepared by self-assembly method, and their diameter was 227 nm. mPEG-b-P(C7-co-CA) micelles could regulate the cell cycle and inhibit the proliferation of 143B cells, which was demonstrated by flow cytometry analysis, CCK-8 assay and 5-Ethynyl-2′-deoxyuridine (EdU) staining. The wound-healing assay and transwell assay showed that mPEG-b-P(C7-co-CA) micelles effectively inhibited the migration and invasion of 143B cells. It was proven that mPEG-b-P(C7-co-CA) micelles downregulated the levels of proliferation and apoptosis-related proteins and affected osteosarcoma migration and invasion by inhibiting the epithelial-mesenchymal transition (EMT). In addition, mPEG-b-P(C7-co-CA) micelles can also inhibit the transcriptional activity of the PI3K/Akt signaling pathway. Therefore, these findings provide new evidence for the pharmacological effects of mPEG-b-P(C7-co-CA) micelles.