This study aimed to evaluate the association between sleep duration and hypertension among adults in southwest China. Baseline variables were collected from a representative sample of 20,053 adults aged 23–98 years in southwest China who received physical examinations from January 2019 to December 2020. All participants were categorized into either a hypertension group or a non-hypertension group. Sleep duration was classified as short (8 h/day). Baseline variables were compared between individuals with and without hypertension by rank-sum tests for two independent samples or χ² tests for nonparametric data. Multivariate logistic regression analysis was performed to evaluate the association between sleep duration and hypertension. The overall incidence of hypertension was 51.2%. Unadjusted analysis showed that the risk of hypertension was higher in individuals with short (8h/day) sleep durations compared with those with a normal (6–8 h/day) sleep duration. The risk of hypertension was significantly increased by 30.1% in participants with a long (>8h/day) sleep duration compared with those with a normal (6–8h/day) sleep duration (OR = 1.301, P < 0.010, 95%CI = 1.149–1.475). The risk of hypertension was also increased by 1.1% in participants with a short (<6h/day) sleep duration compared with participants with a normal (6–8h/day) sleep duration, but the difference was not significant (OR = 1.011, P = 0.849, 95%CI = 0.905–1.129). After fully adjusting for confounding factors (model 4), the risk of hypertension was increased significantly (by 25%) in individuals with a short (<6h/day) sleep duration (OR = 1.25, P = 0.02, 95%CI = 1.036–1.508) but not in those with a long (>8h/day) sleep duration (17.5% increase) compared with participants with a normal (6–8h/day) sleep duration (OR = 1.175, P = 0.144, 95%CI = 0.946–1.460). The results of this study indicate that a short (<6h/day) sleep duration is related to an increased risk of hypertension, suggesting that sleep helps to protect against hypertension.

Pirarubicin (THP) is one of the most commonly used antineoplastic drugs in clinical practice. However, its clinical application is limited due to its toxic and heart‑related side effects. It has been reported that oxidative stress, inflammation and apoptosis are closely associated with cardiotoxicity caused by pirarubicin (CTP). Additionally, it has also been reported that scutellarein (Sc) exerts anti‑inflammatory, antioxidant, cardio‑cerebral vascular protective and anti‑apoptotic properties. Therefore, the present study aimed to investigate the effect of food therapy with Sc on CTP and its underlying molecular mechanism using echocardiography, immunofluorescence, western blot, ROS staining, and TUNEL staining. The in vivo results demonstrated that THP was associated with cardiotoxicity. Additionally, abnormal changes in the expression of indicators associated with oxidative stress, ferroptosis and apoptosis were observed, which were restored by Sc. Therefore, it was hypothesized that CTP could be associated with oxidative stress, ferroptosis and apoptosis. Furthermore, the in vitro experiments showed that Sc and the NADPH oxidase 2 (NOX2) inhibitor, GSK2795039 (GSK), upregulated glutathione peroxidase 4 (GPX4) and inhibited THP‑induced oxidative stress, apoptosis and ferroptosis. However, cell treatment with the ferroptosis inhibitor, ferrostatin‑1, or inducer, erastin, could not significantly reduce or promote, respectively, the expression of NOX2. However, GSK significantly affected ferroptosis and GPX4 expression. Overall, the results of the present study indicated that food therapy with Sc ameliorated CTP via inhibition of apoptosis and ferroptosis through regulation of NOX2‑induced oxidative stress, thus suggesting that Sc may be a potential therapeutic drug against CTP.

Pirarubicin (THP) is one of the classic chemotherapy drugs for cancer treatment. It is often clinically limited because of its cardiotoxicity. The occurrence and development of THP-mediated chemotherapy-related cardiotoxicity (CRC) may be reversed by RING finger protein 10 (RNF10). This study was performed with the aim of evaluating the inhibitory effect of RNF10 on THP-mediated CRC and its molecular mechanism. In vivo, we found that the expression of RNF10 decreased in THP-induced CRC rats, accompanied by Meox2 inhibition and AP-1 activation, resulting in increased cardiomyocyte apoptosis. After small interfering RNA (siRNA) and lentivirus transfection (Lv) of RNF10 in vitro, the expression of RNF10, Meox2, and AP-1 proteins and the degree of cardiomyocyte apoptosis were detected. We found that overexpression of RNF10 in H9C2 cardiomyocytes significantly promoted Meox2 and inhibited AP-1, alleviated apoptosis, and showed further inhibitory activity on THP-induced cardiomyocyte toxicity. Silencing RNF10 showed the opposite result. Our study showed that RNF10 inhibited THP-induced CRC through the activity of Meox2 and AP-1 proteins. RNF10 may be the next drug target for the treatment of CRC and other related cardiovascular diseases.

Background: This study aimed to investigate the correlation between calcific aortic valve disease (CAVD) and carotid artery elasticity using ultra-fast pulse wave velocity (UFPWV) technology. Early detection of alterations in carotid artery elasticity, coupled with the prompt implementation of intervention strategies, can effectively decrease the incidence of cardiovascular diseases. Methods: Patients with CAVD were recruited from the University-Town Hospital of Chongqing Medical University and placed in the observation group. Meanwhile, an equivalent number of patients with non-calcified aortic valve disease were recruited as controls. All participants underwent comprehensive health assessments, including measurements of blood lipids, fasting blood sugar, and other biochemical indicators. Additionally, bilateral carotid intima-media thickness (CIMT) was measured, as well as pulse wave velocity (PWV) at the beginning of systole (PWV-BS) and the end of systole (PWV-ES). Differences in various indicators between the two groups were analyzed, and the factors associated with CAVD and carotid artery elasticity were investigated. The correlation between CAVD and carotid artery elasticity was also evaluated. Results: Patients with CAVD exhibited significantly higher CIMT, PWV-BS, and PWV-ES levels than those with non-calcified aortic valve disease (p < 0.01). PWV-BS and PWV-ES showed progressive increases according to the severity of calcification. Coronary atherosclerotic heart disease and PWV-BS were all identified as independent risk factors for CAVD. The risk factors associated with PWV-BS include hypertension, coronary atherosclerotic heart disease, total cholesterol, and homocysteine (p < 0.05 for all). The risk factors related to PWV-ES include hypertension, coronary atherosclerotic heart disease, total cholesterol, and glycated hemoglobin (p < 0.05 for all). Conclusions: UFPWV technology is a novel method for the early diagnosis of carotid elasticity. Evaluating carotid artery atherosclerosis in patients with CAVD may lead to earlier detection and intervention and reduce the incidence of cardiovascular events.