Summary Based on the use of Osteoporosis Self-Assessment Tool for Asians (OSTA) to assess osteoporosis risk, we found that short sleep duration and taking a daytime nap had an increased risk of osteoporosis. Purpose To explore the associations between different sleep patterns with osteoporosis. Methods 3659 postmenopausal women (average age of 60 years) were divided into low, middle, and high osteoporosis risk categories based on the Osteoporosis Self-Assessment Tool for Asians (OSTA). After having collected by a standard questionnaire, total and nocturnal sleep duration was collapsed to form categories of ≤ 6 h, > 6 h and ≤ 7 h, > 7 h and ≤ 8 h, > 8 h and ≤ 9 h, > 9 h, and daytime nap duration of 0 h and > 0 h. Results As a categorical variable, the total sleep duration of ≤ 6 h per day (OR = 1.34, 95% CI 1.04–1.72), nocturnal sleep duration of ≤ 6 h per night (OR = 1.65, 95% CI 1.24–2.18), and taking a daytime nap (OR = 1.33, 95% CI 1.09–1.64) had higher osteoporosis risk after adjustment for covariates. As a continuous variable, after the adjustment for covariates, both longer total (OR = 0.86, 95% CI 0.78–0.94) and nocturnal sleep duration (OR = 0.83, 95% CI 0.76–0.91) had lower risk of osteoporosis risk while taking longer daytime nap (OR = 1.10, 95% CI 1.02–1.19) had higher osteoporosis risk. Conclusions Postmenopausal women with both short total and nocturnal sleep duration (6 h or less) and taking a daytime nap had increased osteoporosis risk as assessed by OSTA.

Although doxorubicin (DOX) is a potent chemotherapeutic agent, its clinical use is limited by dose-dependent cardiotoxicity. Doxorubicin-induced cardiotoxicity (DIC) promotes cardiomyocyte apoptosis, which leads to cardiac dysfunction, remodeling, and even heart failure. Although Finerenone (Fin), a selective mineralocorticoid receptor antagonist, has demonstrated benefit in the treatment of heart failure, its role in DIC remains unclear. Our study found that Finerenone mitigated myocardial injury, cardiac dysfunction, fibrosis, and remodeling by attenuating DOX-induced cardiomyocyte apoptosis, and it improved survival in a DIC mouse model. Similarly, Finerenone reduced injury and apoptosis in DOX-treated H9c2 cells. We identified key targets of Finerenone in DIC using proteomics and network pharmacology and demonstrated that it prevented the upregulation of p38 phosphorylation induced by DOX. Through in vitro experiments, we confirmed that TAK1-p38 played a critical role in mediating the protective effects of Finerenone against DIC. Furthermore, we found that Finerenone inhibits TAK1-p38 phosphorylation and cardiomyocyte apoptosis by antagonizing MR to suppress ROS. Overall, these results suggested that Finerenone ameliorated DIC primarily by inhibiting cardiomyocyte apoptosis via the TAK1-p38 pathway. Our findings elucidate a key mechanism underlying the cardioprotective effect of Finerenone in DIC and provide a theoretical basis for expanding its clinical applications.