Ferroptosis, a unique type of cell death, is characterized by iron-dependent accumulation and lipid peroxidation. It is closely related to multiple biological processes, including iron metabolism, polyunsaturated fatty acid metabolism, and the biosynthesis of compounds with antioxidant activities, including glutathione. In the past 10 years, increasing evidence has indicated a potentially strong relationship between ferroptosis and the onset and progression of age-related orthopedic diseases, such as osteoporosis and osteoarthritis. Therefore, in-depth knowledge of the regulatory mechanisms of ferroptosis in age-related orthopedic diseases may help improve disease treatment and prevention. This review provides an overview of recent research on ferroptosis and its influences on bone and cartilage homeostasis. It begins with a brief overview of systemic iron metabolism and ferroptosis, particularly the potential mechanisms of ferroptosis. It presents a discussion on the role of ferroptosis in age-related orthopedic diseases, including promotion of bone loss and cartilage degradation and the inhibition of osteogenesis. Finally, it focuses on the future of targeting ferroptosis to treat age-related orthopedic diseases with the intention of inspiring further clinical research and the development of therapeutic strategies.
Peritendinous adhesion formation (PAF) can substantially limit the range of motion of digits. However, the origin of myofibroblasts in PAF tissues is still unclear. In this study, we found that the concentration of active TGF-β1 and the numbers of macrophages, mesenchymal stromal cells (MSCs), and myofibroblasts in human and mouse adhesion tissues were increased. Furthermore, knockout of TGF-β1 in macrophages or TGF-β1R2 in MSCs inhibited PAF by reducing MSC and myofibroblast infiltration and collagen I and III deposition, respectively. Moreover, we found that MSCs differentiated into myofibroblasts to form adhesion tissues. Systemic injection of the TGF-β–neutralizing antibody 1D11 during the granulation formation stage of PAF significantly reduced the infiltration of MSCs and myofibroblasts and, subsequently, PAF. These results suggest that macrophage-derived TGF-β1 recruits MSCs to form myofibroblasts in peritendinous adhesions. An improved understanding of PAF mechanisms could help identify a potential therapeutic strategy.
Osteoarthritis (OA) in China is gradually becoming an important scientific research area that has had a significant impact on research and development (R&D) activities in the OA field worldwide. This article summarizes the R&D progress related to OA in China in recent years. The National Natural Science Foundation of China (NSFC) is a national funding institution for basic research and plays a critical role in promoting and supporting Chinese scholars’ R&D activities. We collected and analyzed information on NSFC funding in the field of OA from 2010 to 2019, including the amount, the level and the program categories of the funded projects. The data fully demonstrate the important and positive role of the NSFC in supporting free exploration, cultivating research teams and young talent, and boosting OA R&D. In this article, we outline and discuss hot topics in focused areas, key advances in this field and the prospects for progress in OA research in China.
Metastasis of tumor cells from primary tumor and growth at secondary sites are the major cause of mortality in cancer patients. This event may occur years and even decades after successful removal of the primary tumor and adjuvant therapy. Relapse and metastasis are universally existed in various malignancies. This phenomenon is attributed to a small amount of residual tumor cells remained in host for years, which is called as dormancy. Tumor dormancy is characterized by the balanced cell proliferation and cell death, immune evasion from host, non-angiogenic feature, insufficiency of metastatic capacity, cell cycle arrest as well as resistant to conventional chemotherapy. The molecular expressing profile suggested that dormancy is a state of quiescent cancer stem-like cells (CSCs), which are more resistant to chemotherapy and targeted therapy. Hitherto, the progression on tumor dormancy is relatively slow because there are no proper experimental models and biomarkers for identifying the dormant cells. It is no doubt that clarifying the regulatory mechanism of enter or exit of dormancy will help scientists to develop targeted strategy for eliminating dormant tumor cells, and then hinder the distant relapse and metastasis for various malignancies. This review focuses on tumor dormancy, the association of tumor dormancy with CSCs and strengthens the angiogenic switch for enter or exit of dormancy. It enlightens researchers to explore and develop more specific targeted drugs for clearance of the relapse danger.
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