Editorial: Role and mechanism of regulated cell death in musculoskeletal development, homeostasis, and diseases

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extracellular or intracellular environment when adaptive responses are insufficient. Given its crucial role in pathophysiological processes and the controllability of its molecular mechanisms, RCD has garnered significant attention in the field of cell death research, emerging as a highly popular and promising research direction. Since 1970s, numerous forms of RCD have been identified, such as ferroptosis, cuproptosis, apoptosis, autophagy-dependent cell death, lysosome-dependent cell death, mitochondrial permeability transition-driven necrosis, oxeiptosis, entotic cell death, necroptosis, NETotic cell death, alkaliptosis, parthanatos, pyroptosis, immunogenic cell death, and PANoptosis.Musculoskeletal disorders are the primary source of disability worldwide, resulting in immense human distress and substantial socioeconomic costs. The musculoskeletal system consists of bones, skeletal muscles, joints, and associated tissues. It performs many vital functions, such as enabling mechanical movement, supporting body weight, maintaining posture and body shape, storing minerals, functioning as hematopoiesis, and protecting internal organs. These functions depend on the good quality and adequate quantity of cells within the musculoskeletal system. But aging and et al.). In OA pathogenesis, the central event is the degeneration of articular cartilage, which is maintained by chondrocytes and their ability to balance the synthesis and degradation of extracellular matrix. OA is a multifactorial degenerative joint disease influenced by a combination of genetic, biomechanical, and environmental factors. Key contributors include aging, joint injury, obesity, and abnormal joint loading. These factors elevate ROS production, reduce chondrocyte autophagy, promote chondrocyte apoptosis, and upregulate matrix-degrading enzyme. This perturbs the catabolic and anabolic balance in cartilage, contributing to cartilage degeneration, joint inflammation, and subsequent bone remodeling. These changes hinder the proper transmission of mechanical loads to chondrocyte, amplifying cell death of chondrocyte and ultimately resulting in the occurrence and progression of OA (Li et al.). Recent results from bioinformatic prediction and in vitro studies revealed that cuproptosis may also play important roles in RA, IVDD, and OA (Xiang et al.). In addition, many other RCD modes or their cross-talks have been proved to be implicated in the development and progression of above and other musculoskeletal diseases. Despite these insights, significant gaps remain in in our understanding of the exact mechanisms and roles of RCD in musculoskeletal diseases. Bridging these gaps is essential for the development of effective prevention and treatment strategies, which will ultimately enhance the outcomes for patients suffering from musculoskeletal diseases.

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