Aims: In light of the escalating global incidence of Parkinson’s disease and the dearth of therapeutic interventions that can alter the disease’s course, there exists an urgent necessity to comprehensively elucidate and quantify the disease’s global burden.Methods: This study analyzed the incidence, prevalence, and disability-adjusted life years (DALYs) of Parkinson’s disease at global, regional, and national levels based on the Global Burden of Disease Study 2021. Bayesian age-period cohort (BAPC) analysis was used to predict the burden in Parkinson’s disease from 2022 to 2035.Results: In 2021, 11.77 million people worldwide had Parkinson’s disease. Age-standardized rates of incidence, prevalence, and DALYs increased to 15.63/100,000, 138.63/100,000, and 89.59/100,000. The burden of Parkinson’s disease were higher in males than in females, and showed an increase and then a slight decrease with age. The disease burden was highest in East Asia. BAPC projection showed an increase in all metrics by 2035 except for a slight decrease in the age-standardized DALYs rates.Conclusion: The global burden of Parkinson’s disease has risen over the past 32 years, and there is a need to focus on key populations, as well as to improve health policies to prevent and treat Parkinson’s disease.

Osteoarthritis is a major cause of disability worldwide, and understanding epidemiological trends in osteoarthritis is critical for public health planning and intervention strategies. This study analyzed the global, regional, and national burden on osteoarthritis utilizing the Global Burden of Disease Study 2021. Trends from 1990 to 2021 were primarily assessed, with projections to 2050 based on demographic changes and historical data. In 2021, 607 (95% UI: 538–671) million people worldwide suffered from osteoarthritis, including 46.6 (95% UI: 41.1–51.6) million new cases, and the DALYs was 21.3 (95% UI: 10.2–42.9) million. Age-standardized incidence, prevalence and DALYs rates increased to 535.00/100,000 (95% UI: 472.38–591.97), 6967.29/100,000 (95% UI: 6180.70–7686.06), and 244.50/100,000 (95% UI: 117.06–493.11), with knee osteoarthritis accounting for more than 56%. Age-standardized rates of osteoarthritis were higher in females than in males. East Asia, South Asia, and Western Europe were the regions and China, India, and the United States were the countries with the highest burdens. In addition, high body-mass index led to 4.43 (95% UI: -0.42–12.34) million DALYs, with an increase of 205.10%. Bayesian age-period cohort projections showed that the burden of osteoarthritis would continue to rise from 2021 to 2050. As an ageing population and rising obesity rates, the burden of osteoarthritis will continue to rise, with females and the middle-aged and older age groups being the current populations of concern. Awareness-raising, early detection, and effective management are essential to reduce the burden of osteoarthritis in the coming decades, especially among vulnerable groups.

Fluorine is widely dispersed in nature and has multiple physiological functions. Although it is usually regarded as an essential trace element for humans, this view is not held universally. Moreover, chronic fluorosis, mainly characterized by skeletal fluorosis, can be induced by long-term excessive fluoride consumption. High concentrations of fluoride in the environment and drinking water are major causes, and patients with skeletal fluorosis mainly present with symptoms of osteosclerosis, osteochondrosis, osteoporosis, and degenerative changes in joint cartilage. Etiologies for skeletal fluorosis have been established, but the specific pathogenesis is inconclusive. Currently, active osteogenesis and accelerated bone turnover are considered critical processes in the progression of skeletal fluorosis. In recent years, researchers have conducted extensive studies in fields of signaling pathways (Wnt/β-catenin, Notch, PI3K/Akt/mTOR, Hedgehog, parathyroid hormone, and insulin signaling pathways), stress pathways (oxidative stress and endoplasmic reticulum stress pathways), epigenetics (DNA methylation and non-coding RNAs), and their inter-regulation involved in the pathogenesis of skeletal fluorosis. In this review, we summarised and analyzed relevant findings to provide a basis for comprehensive understandings of the pathogenesis of skeletal fluorosis and hopefully propose more effective prevention and therapeutic strategies.

Increasing attention has recently been paid to the harm of polycystic ovary syndrome (PCOS) to women. However, due to the inconsistency of global clinical diagnostic standards and the differing allocation of medical resources among different regions, there is a lack of comprehensive estimation of the global incidence and disability-adjusted life years (DALYs) of PCOS. Thus, it is difficult to assess the disease burden. We extracted PCOS disease data from 1990 to 2019 from the Global Burden of Disease Study (GBD) 2019 and estimated the incidence, DALYs, and the corresponding age-standardized rates (ASRs) of PCOS, as well as the socio-demographic index (SDI) quintiles, to describe epidemiological trends at the global level, encompassing 21 regions and 204 countries and territories. Globally, the incidence and DALYs of PCOS have increased. Its ASR also shows an increasing trend. Among them, the high SDI quintile seems relatively stable, whereas other SDI quintiles are constantly rising over time. Our research has provided clues regarding the disease pattern and epidemic trend of PCOS and analyzed the possible causes of disease burden in some specific countries and territories, which may have some value in health resource allocation and health policy formulation and prevention strategies.

Background: As a central organ of energy metabolism, the liver is closely related to selenium for its normal function and disease development. However, the underlying roles of mitochondrial energy metabolism and mitophagy in liver fibrosis associated with selenium remain unclear. Methods: 28 rats were randomly divided into normal, low-selenium, nano-selenium supplement-1, and supplement-2 groups for a 12-week intervention. We observed pathological and ultrastructural changes in the liver and analyzed the effects of selenium deficiency and nano-selenium supplementation on liver metabolic activities and crucial proteins expression of mammalian target of the rapamycin (mTOR) signaling pathway. Results: Selenium deficiency caused liver pathological damage and fibrosis with the occurrence of mitophagy by disrupting normal metabolic activities; meanwhile, the mTOR signaling pathway was up-regulated to enhance mitophagy to clear damaged mitochondria. Furthermore, nano-selenium supplements could reduce the severity of pathological damage and fibrosis in livers and maintain normal energy metabolic activity. With the increased concentrations of nano-selenium supplement, swelling mitochondria and mitophagy gradually decreased, accompanied by the higher expression of mTOR and phosphorylation-modified mTOR proteins and lower expression of unc-51 like autophagy activating kinase 1 (ULK1) and phosphorylation-modified ULK1 proteins. Conclusions: Mitophagy regulated by the mTOR signaling pathway plays a dual protective role on low-selenium inducing liver fibrosis and nano-selenium supplements preventing liver fibrosis. Mitochondrial energy metabolism plays an important role in these processes as well.