Research findings reveal that thermal environments precisely regulate the skeletal system through a triple regulation of “structural morphology-cellular dynamics-molecular mechanisms”: At the tissue morphology level, moderate heat exposure can promote increased bone density and longitudinal growth, as well as improved fracture load and yield point, but may negatively affect geometric shape and cortical bone thickness. Continuous high-temperature exposure harms bone structure, manifested as changes in biomechanical characteristics such as decreased toughness and rigidity. At the cellular level, thermal environments directly affect the proliferation/apoptosis balance of osteoblasts and osteoclasts, and by regulating osteocyte network activity and bone marrow mesenchymal stem cell fate decisions, these four cell populations form temperature-dependent metabolic regulatory circuits. At the molecular dimension, heat stress can activate the release of neural factors such as CGRP and NPY, which possess dual regulatory functions promoting both bone formation and resorption; simultaneously achieving coordinated regulation of angiogenesis and fat inhibition through VEGF and TGFβ. The thermal environment–bone regulatory mechanisms revealed in this study have important translational value: they not only provide theoretical basis for biomechanical protection strategies for high-temperature workers and athletes, but also offer innovative entry points for analyzing the pathological mechanisms of heat stroke secondary bone injury and osteoporosis through heat stress-related signaling pathways, while establishing a theoretical foundation for the development of temperature-responsive functionalized biomaterials in bone tissue engineering.

Muscle stem cells (MuSCs) are the key to muscle regeneration. The activation and maintenance of MuSCs require the precise regulation of their microenvironments. Myofibers and other cells including endothelial cells, fibroblasts, and immune cell populations constitute the cell components of the MuSC niche. The communication between these cell populations and MuSCs play an essential role in muscle repair. Furthermore, the physical and chemical stimulations around MuSCs also affect the cell behaviors of MuSCs. Extracellular matrix (ECM) and the factors stored in it generate a repair-promoting niche for efficient muscle regeneration. Understanding the mechanism of muscle stem cell regulation is the basis of clinically optimizing muscle repair. In this review, we discuss recent findings about the microenvironments of MuSCs and their functions in muscle regeneration, which would shed light on new targets and strategies for muscle injury treatment.

Sclerostin (SOST) is a specific osteocyte protein. During the differentiation and proliferation of osteoblasts and osteoclasts, the high expression of SOST can inhibit bone formation and contribute to osteoporosis and the bone metastasis of malignant tumors. Most of the research on SOST has focused on bone cells, but studies have found that SOST is not a specific product of bone cells but that it is also expressed by articular chondrocytes. SOST can regulate the progression of osteoarthritis in bone and cartilage, promote subchondral bone sclerosis, and inhibit cartilage degeneration. A review of the literature found that SOST can not only regulate bone metabolism, but it is also expressed in cardiovascular, kidney, liver, and other tissues, influencing the occurrence and development of diseases in these organs and tissues. Studies have found that diseases of extra-bone organs, such as atherosclerosis, aneurysm, chronic kidney disease, and cirrhosis, may be related to the expression of SOST. Simultaneously, long-term exercise can reduce SOST levels, especially in areas of high bone strain. Prolonged exercise induces bone adaptation to mechanical stress, resulting in diminished responsiveness of bone cells to exercise and a reduction in serum SOST levels. Short-term acute exercise can elevate serum SOST levels, but these results are often limited by age, gender, and energy status. In general, serum SOST rises immediately after short-term acute exercise, returning to baseline or even decreasing after exercise.