Osteoporosis is becoming a major concern in the field of public health. The process of bone loss is insidious and does not directly induce obvious symptoms. Complications indicate an irreversible decrease in bone mass. The high-risk populations of osteoporosis, including postmenopausal women, elderly men, diabetic patients and obese individuals need regular bone mineral density testing and appropriate preventive treatment. However, the primary changes in these populations are different, increasing the difficulty of effective treatment of osteoporosis. Determining the core pathogenesis of osteoporosis helps improve the efficiency and efficacy of treatment among these populations. Oxidative stress is a common pathological state secondary to estrogen deficiency, aging, hyperglycemia and hyperlipemia. In this review, we divided oxidative stress into the direct effect of reactive oxygen species (ROS) and the reduction of antioxidant enzyme activity to discuss their roles in the development of osteoporosis. ROS initiated mitochondrial apoptotic signaling and suppressed osteogenic marker expression to weaken osteogenesis. MAPK and NF-κB signaling pathways mediated the positive effect of ROS on osteoclast differentiation. Antioxidant enzymes not only eliminate the negative effects of ROS, but also directly participate in the regulation of bone metabolism. Additionally, we also described the roles of proinflammatory factors and HIF-1α under the pathophysiological changes of inflammation and hypoxia, which provided a supplement of oxidative stress-induced osteoporosis. In conclusion, our review showed that oxidative stress was a common pathological state in a high-risk population for osteoporosis. Targeted oxidative stress treatment would greatly optimize the therapeutic schedule of various osteoporosis treatments.

In recent decades, the mechanism underlying bone metabolic disorders based on energy metabolism has been heavily researched. Bone resorption by osteoclasts plays an important role in the occurrence and development of osteoporosis. However, the mechanism underlying the osteoclast energy metabolism disorder that interferes with bone homeostasis has not been determined. Bone resorption by osteoclasts is a process that consumes large amounts of adenosine triphosphate (ATP) produced by glycolysis and oxidative phosphorylation. In addition to glucose, fatty acids and amino acids can also be used as substrates to produce energy through oxidative phosphorylation. In this review, we summarize and analyze the energy-based phenotypic changes, epigenetic regulation, and coupling with systemic energy metabolism of osteoclasts during the development and progression of osteoporosis. At the same time, we propose a hypothesis, the compensatory recovery mechanism (involving the balance between osteoclast survival and functional activation), which may provide a new approach for the treatment of osteoporosis.

Osteoporosis is a common bone metabolic disease that causes a heavy social burden and seriously threatens life. Improving osteogenic capacity is necessary to correct bone mass loss in the treatment of osteoporosis. Osteoblasts are derived from the differentiation of bone marrow mesenchymal stem cells, a process that opposes adipogenic differentiation. The peroxisome proliferator‑activated receptor γ and Wnt/β‑catenin signaling pathways mediate the mutual regulation of osteogenesis and adipogenesis. Lipid substances play an important role in the occurrence and development of osteoporosis. The content and proportion of lipids modulate the activity of immunocytes, mainly macrophages, and the secretion of inflammatory factors, such as IL‑1, IL‑6 and TNF‑α. These inflammatory effectors increase the activity and promote the differentiation of osteoclasts, which leads to bone imbalance and stronger bone resorption. Obesity also decreases the activity of antioxidases and leads to oxidative stress, thereby inhibiting osteogenesis. The present review starts by examining the bidirectional differentiation of BM‑MSCs, describes in detail the mechanism by which lipids affect bone metabolism, and discusses the regulatory role of inflammation and oxidative stress in this process. The review concludes that a reasonable adjustment of the content and proportion of lipids, and the alleviation of inflammatory storms and oxidative damage induced by lipid imbalances, will improve bone mass and treat osteoporosis.

Background: Multiple studies have shown that an imbalance in the intestinal microbiota is related to bone metabolism, but the role of the intestinal microbiota in postmenopausal osteoporosis remains to be elucidated. We explored the effect of the intestinal microbiota on osteoporosis. Methods: We constructed a postmenopausal osteoporosis mouse model, and Micro CT was used to observe changes in bone structure. Then, we identified the abundance of intestinal microbiota by 16S RNA sequencing and found that the ratio of Firmicutes and Bacteroidetes increased significantly. UHPLC-MS analysis was further used to analyze changes in metabolites in feces and serum. Results: We identified 53 upregulated and 61 downregulated metabolites in feces and 2 upregulated and 22 downregulated metabolites in serum under OP conditions, and interestedly, one group of bile acids showed significant differences in the OP and control groups. Network analysis also found that these bile acids had a strong relationship with the same family, Eggerthellaceae. Random forest analysis confirmed the effectiveness of the serum and fecal models in distinguishing the OP group from the control group. Conclusions: These results indicated that changes in the gut microbiota and metabolites in feces and serum were responsible for the occurrence and development of postmenopausal osteoporosis. The gut microbiota is a vital inducer of osteoporosis and could regulate the pathogenesis process through the “microbiota-gut-metabolite-bone” axis, and some components of this axis are potential biomarkers, providing a new entry point for the future study on the pathogenesis of postmenopausal osteoporosis.

Postmenopausal osteoporosis is a prevalent metabolic bone disorder characterized by a decrease in bone mineral density and deterioration of bone microstructure. Despite the high prevalence of this disease, no effective treatment for osteoporosis has been developed. Exercise has long been considered a potent anabolic factor that promotes bone mass via upregulation of myokines secreted by skeletal muscle, exerting long‐term osteoprotective effects and few side effects. Irisin was recently identified as a novel myokine that is significantly upregulated by exercise and could increase bone mass. However, the mechanisms underlying exercise‐induced muscle‐bone crosstalk remain unclear. Here, we identified that polyunsaturated fatty acids (arachidonic acid and docosahexaenoic acid) are increased in skeletal muscles following a 10‐week treadmill exercise programme, which then promotes the expression and release of FNDC5/irisin. In osteoblasts, irisin binds directly to Cav1, which recruits and interacts with AMP‐activated protein kinase α (AMPKα) to activate the AMPK pathway. Nrf2 is the downstream target of the AMPK pathway and increases the transcription of HMOX1 and Fpn. HMOX1 is involved in regulating the cell cycle and promotes the proliferation of osteoblasts. Moreover, upregulation of Fpn in osteoblasts enhanced iron removal, thereby suppressing ferroptosis in osteoblasts. Additionally, we confirmed that myotube‐derived exosomes are involved in the transportation of irisin and enter osteoblasts through caveolae‐mediated endocytosis. In conclusion, our findings highlight the crucial role of irisin, present in myotube‐derived exosomes, as a crucial regulator of exercise‐induced protective effects on bone, which provides novel insights into the mechanisms underlying exercise‐dependent treatment of osteoporosis.

Background: COVID-19 is currently rampant in China, causing unpredictable harm to humans. This study aimed to quantitatively and qualitatively investigate the research trends on coronaviruses using bibliometric analysis to identify new prevention strategies. Methods: All relevant publications on coronaviruses were extracted from 2000–2020 from the Web of Science database. An online analysis platform of literature metrology, bibliographic item co-occurrence matrix builder (BICOMB) and CiteSpace software were used to analyse the publication trends. VOSviewer was used to analyse the keywords and research hotspots and compare COVID-19 information with SARS and MERS information. Results: We found a total of 9,760 publications related to coronaviruses published from 2000 to 2020. The Journal of Virology has been the most popular journal in this field over the past 20 years. The United States maintained a top position worldwide and has provided a pivotal influence, followed by China. Among all the institutions, the University of Hong Kong was regarded as a leader for research collaboration. Moreover, Professors Yuen KY and Peiris JSM made great achievements in coronavirus research. We analysed the keywords and identified 5 coronavirus research hotspot clusters. Conclusions: We considered the publication information regarding different countries, institutions, authors, journals, etc. by summarizing the literature on coronaviruses over the past 20 years. We analysed the studies on COVID-19 and the SARS and MERS coronaviruses. Notably, COVID-19 must become the research hotspot of coronavirus research, and clinical research on COVID-19 may be the key to defeating this epidemic.