Our previous study has found that miPEP31, which is encoded by pri-miRNA-31, inhibits the transcription of pri-miRNA-31 and alleviates angiotensin (Ang) II-induced hypertension. miR-31 is involved in proliferation of primary vascular smooth muscle cells (VSMCs), the key functional cells involved in hypertensive vascular remodeling. However, the role and mechanism of miPEP31 in the proliferation of VSMCs remain unclear. The aim of this study is to investigate whether miPEP31 plays an important role in VSMC proliferation and contributes to vascular remodeling. We found that the administration of synthetic miPEP31 mitigated but miPEP31 deficiency aggravated the Ang II-induced aortic thickness of intima plus media and fibrotic area. miPEP31 is endogenously expressed and penetrates into nuclei in VSMCs. miPEP31 inhibits PDGF-BB-induced VSMC proliferation in a dose-dependent manner and decreases the Ang Ⅱ-induced aortic α-SMA staining area. Mechanistically, we demonstrated that miPEP31 acts as a transcriptional repressor and inhibits miR-31 expression by cooperating with Trps1, a GATA family zinc finger transcription factor. In summary, our study suggests that miPEP31 protects against vascular remodeling in Ang II-infused mice via cooperation with transcription factor Trps1 to inhibit miR-31 expression and, subsequently, VSMC proliferation. This finding highlights the therapeutic effect and role of miPEP31 on hypertensive target organs and functional cells.

This study investigated the association between several dietary quality scores-including the healthy eating index-2015(HEI-2015), dietary inflammatory index (DII), and dietary approaches to stop hypertension (DASH)-and the risk of cardiovascular disease(CVD) mortality in hypertension treatment group.

Psychological problems such as anxiety and depression in children show an increasing prevalence, but low treatment rates and few interventions have been implemented. The relationship between combined exercise and psychological interventions on anxiety, depression, and blood pressure in children has not been clearly studied. The aim of this study was to investigate the effects of a combined psychological and exercise intervention program on children's anxiety and depression conditions and blood pressure.

Hypertension is a major contributor to the global burden of disease and increased mortality in the general population. Currently, the etiology and pathogenesis of hypertension are not fully understood. Emerging evidence suggests an association between aspartate aminotransferase (AST) and hypertension, but whether this relationship is causal remains unclear.

This prospective cohort study investigated the association between the albumin to serum creatinine ratio (sACR) and heart failure (HF) incidence in 150 chronic kidney disease (CKD) patients. Over a median 23-month follow-up, 114 HF events occurred. Multivariate Cox regression revealed a higher HF risk in the lowest versus highest sACR tertile (adjusted HR=1.742, 95% CI=1.341-2.002, p=0.023). Lower sACR correlated with worsened cardiac structure/function. The predictive AUC for HF was 0.64 for sACR alone and improved to 0.79 when combined with clinical covariates. We conclude that low sACR is independently associated with increased HF incidence in CKD patients.

Myocardial infarction (MI) is a leading cause of morbidity and mortality globally, primarily due to oxidative stress-induced cardiomyocyte apoptosis and adverse cardiac remodeling. OL-FS13, a neuroprotective peptide derived from Odorrana livida, has previously shown anti-apoptotic effects in cerebral ischemia models. However, its role in myocardial protection remains unclear. In this study, we investigated the cardioprotective effects of OL-FS13 in both in vitro and in vivo models of MI. Hydrogen peroxide (H₂O₂) was used to induce oxidative stress in primary neonatal rat cardiomyocytes, while permanent ligation of the left anterior descending (LAD) coronary artery was employed to establish a murine MI model. OL-FS13 treatment significantly attenuated cardiomyocyte apoptosis, reduced ROS accumulation, improved left ventricular function, and decreased infarct size. Mechanistically, OL-FS13 activated the Nrf2/HO-1 signaling pathway, restoring antioxidant protein levels and suppressing oxidative stress-induced apoptosis. Pharmacological inhibition of Nrf2 with ML385 abrogated the antioxidant and anti-apoptotic effects of OL-FS13 both in vitro and in vivo, confirming the central role of this pathway. These findings demonstrate that OL-FS13 exerts potent cardioprotective effects via Nrf2/HO-1 pathway activation and ROS suppression, suggesting its potential as a novel therapeutic agent for the treatment of myocardial infarction.

With rapid advancements in genomics, proteomics, and metabolomics researchers have gained significant insights into ACS (ACS) pathogenesis. Studies have revealed specific biomarkers linked to ACS and provided novel tools for risk evaluation and early diagnosis. Genomic breakthroughs have enabled exploration of genetic factors contributing to ACS. Transcriptomics has facilitated the analysis of gene expression alterations in patients with ACS. Proteomics has identified potential therapeutic targets by pinpointing biomarkers, paving the way for new drug development. Advances in metabolomics have enabled monitoring of changes in metabolic pathways, offering valuable information for early diagnosis and disease prognosis. In summary, multiomics research has shed light on the critical aspects of ACS clinical strategies, facilitating advancements in early diagnosis, risk assessment, and personalized therapy, and will increasingly assume a pivotal role in future clinical practice.

Transcatheter adrenal artery embolization (TAAE) has emerged as a minimally invasive technique for selective adrenal ablation, offering potential therapeutic applications for various adrenal disorders. However, its safety profile remains insufficiently characterized. This preclinical study aimed to evaluate the physiological, biochemical, and histological effects of ethanol-based TAAE in a large-animal model.

To evaluate the efficacy of an interdisciplinary care model with family empowerment (ICCM-FE) on clinical and psychosocial outcomes in patients with hypertension and diabetes.

Apical muscular ventricular septal defects (mVSDs) are surgically challenging because of their location. Although transcatheter device closure is effective in many patients, large apical defects in infants present specific technical limitations and risks.

As a gastrointestinal hormone, gastrin stimulates gastric acid secretion and intestinal mucosal nutrition. Evidence links it closely to coronary heart disease, ischemia‒reperfusion injury and hypertension. The relevant literature was systematically retrieved from PubMed, Web of Science, China National Knowledge Infrastructure (CNKI), and other scientific databases, as well as other sources. Gastrin is a polypeptide hormone that is synthesized mainly by G cells in the antrum and proximal small intestine. Its secretion is controlled by neural regulation and humoral regulation. Gastrin is significantly associated with coronary heart disease, cardiac ischemia-reperfusion injury, hypertension and other cardiovascular diseases. The risk of coronary heart disease in patients with high serum gastrin levels is greater than that in the general population, and the serum gastrin level is higher in patients with myocardial infarction, which further suggests that hypergastrinemia may be an important risk factor for CHD. Myocardial cells express CCKBR, and intracoronary gastrin administration improves myocardial contractility through CCKBR. Several studies have shown that gastrin can also protect the myocardium against ischemia-reperfusion injury through the STAT3 signaling pathway. Gastrin may regulate blood pressure through the central nervous system or directly dilate blood vessels. Gastrin can promote the secretion of gastric acid and nutrition of intestinal mucosa. Gastrin exerts cardioprotective effects and regulates the occurrence of hypertension.

This study was designed to elucidate the role of circPcmtd1 in regulating pulmonary artery smooth muscle cells (PASMCs) proliferation and migration, through the HSP90AB1/AKT signaling axis, in rats with high pulmonary blood flow-induced PAH. A rat model of high pulmonary blood flow-induced PAH was established by an abdominal aorta-inferior vena cava shunt surgery. The expression of circPcmtd1 in PASMCs of rats with high pulmonary blood flow-induced PAH was verified by qRT-PCR. The effects of circPcmtd1 on the proliferation and migration of PASMCs were explored by lentiviral transfection, cell proliferation assay, and scratch assay. RNA pull-down assay, mass spectrometric analysis, lentiviral transfection, and western blot were used to explore the molecular mechanisms by which circPcmtd1 regulated the proliferation and migration of PASMCs in rats with high pulmonary blood flow-induced PAH. We found that the expression of circPcmtd1 was down-regulated in PASMCs of rats with high pulmonary blood flow-induced PAH. Functional experiments showed that overexpression of circPcmtd1 inhibited the proliferation and migration of PASMCs. RNA pull-down assay and mass spectrometric analysis revealed that circPcmtd1 could bind to HSP90AB1 protein. Further, we found that high expression of HSP90AB1 could promote the proliferation and migration of PASMCs in rats with high pulmonary blood flow-induced PAH. Mechanistic investigation demonstrated that the binding of circPcmtd1 to HSP90AB1 could regulate the phosphorylation of AKT. In conclusion, circPcmtd1 directly bound to the HSP90AB1 protein to mediate the phosphorylation of AKT, thereby regulating the proliferation and migration of PASMCs.

This retrospective cohort study assessed the predictive value of routine clinical indicators for diabetic nephropathy (DN) in elderly patients (≥60 years) with type 2 diabetes mellitus (T2DM) and hypertension. A total of 102 hospitalized patients (January 2022-December 2023) were divided into DN and non-DN groups. Fasting blood glucose (FBG), 2-h postprandial glucose (2hPG), HbA1c, systolic blood pressure (SBP), urinary microalbumin (UMA), and urinary albumin-to-creatinine ratio (UACR) were analyzed using univariate and multivariate logistic regression to identify independent predictors. A nomogram based on these indicators was developed and evaluated by receiver operating characteristic (ROC) analysis. All six factors independently predicted DN ( < 0.05), with 2hPG showing the strongest association (OR = 8.922). The combined model achieved high predictive accuracy (AUC = 0.906), outperforming any single indicator. This model offers a practical tool for early DN risk stratification in elderly T2DM patients with hypertension, supporting individualized prevention and intervention.

Pulmonary arterial hypertension (PAH) is a group of complex vasculopathies characterized by increased pulmonary arterial pressure and subsequent pulmonary vascular remodeling. However, the underlying pathogenesis of PAH has not been fully elucidated. In the present study, we employed bioinformatics technology to investigate the pathogenesis of PAH. Microarray datasets related to PAH were retrieved from the Gene Expression Omnibus database to screen for ER stress-related genes (ERSRGs) between normal control and PAH samples. The differentially expressed genes (DEGs) were analyzed for functional enrichment and protein‒protein interaction (PPI) networks. DEG-related miRNAs and transcriptional factor (TF) were predicted to construct the miRNA-TF-hub gene network. The diagnostic accuracy of the hub genes was assessed via receiver operating characteristic (ROC) curve analysis. The relative abundances of different types of immune cells were determined via immune infiltration analysis. The screening detected 20 ERSRGs between normal and PAH samples, nine of which (HIF1A, BCL2L1, TLR4, HMOX1, VCAM1, EGR1, MAPK8, LCN2, and CEBPB) were further identified as hub genes via the PPI network. To construct a regulatory network analysis of the Hub genes, 57 miRNAs and 35 TFs were subsequently predicted. There was a significant difference in the infiltration of 17 types of immune cells between the two groups. These results suggest that the nine hub genes might play crucial roles in the development of PAH. These findings might provide new therapeutic targets for PAH or potential biomarkers for its diagnosis.

Hypertension is thought to accelerate biological aging. However, evidence of a causal effect is lacking. This study aimed to provide evidence of a relationship between hypertension and biological aging by analyzing data from the 2005-2010 National Health and Nutrition Examination Survey (NHANES) and by Mendelian randomization (MR).

This study seeks to unravel the effects of trimetazidine (TMZ) on hypertensive nephropathy (HN) in mice and its underlying mechanisms.

The concurrent prevalence of major depression and hypertension represents a significant clinical concern. This study aims to investigate the potential causal relationship among these conditions from a genetic standpoint.

To evaluate the clinical utility of non-invasive hemodynamic indicators in assessing cardiovascular risk among hypertensive patients with coronary atherosclerotic heart disease (CAD), and to explore their correlation with lipid metabolism disorders.

Based on Mendelian randomization (MR) methods, this study aims to explore causal associations of uric acid (UA) levels with aortic aneurysms (AAs).

Hypertension and Alzheimer's disease (AD) are common comorbidities that seriously damage the health of the elderly. This review lays out the complex bidirectional association between hypertension and AD. From a pathological perspective, hypertension can not only indirectly increase the risk of AD through inducing cerebrovascular lesions such as atherosclerosis and stroke but also directly accelerate the core pathological progression of AD, including promoting the accumulation of amyloid-β (Aβ) proteins and the hyperphosphorylation of tau protein. Additionally, various shared modifiable risk factors, such as obesity, sleep disturbances, diet patterns, psychosocial factors etc., are summarized in detail, and their shared pathophysiological pathways, including chronic inflammation, oxidative stress and intestinal dysbiosis, are revealed. This article focuses on exploring the potential of synergistic management: on the one hand, some antihypertensive drugs, such as angiotensin II receptor blockers (ARBs), exhibit neuroprotective effects beyond blood pressure reduction. On the other hand, DASH, Mediterranean and MIND dietary patterns, along with regular physical exercise and positive psychological interventions, have all been proven to reduce the incidence risk of both diseases simultaneously. Digital health technology, such as the LETHE App provides a new paradigm for realizing dynamic monitoring and personalized management of risk factors. This review emphasizes that integrating hypertension prevention and control into the primary prevention strategy for AD and adopting a synergistic management plan that combines lifestyle interventions, medications, and digital technologies is crucial for achieving healthy aging.