Clinical and Experimental Hypertension最新文献

Regular exercise training can significantly improve the gut environment and influence the metabolic activity of the gut microbiota. These changes promote the production of beneficial metabolites, which may modulate blood pressure regulation through multiple mechanisms. The beneficial microbial species including Faecalibacterium prausnitzii, Bifidobacterium spp., Lactobacillus spp., Roseburia spp.,and Bacteroides spp. These beneficial microbes produce various metabolites during metabolism, including short-chain fatty acids, vitamins, lactic acid, bileacids, and gamma-aminobutyric acid. These metabolites are not only essential for maintaining gut health but also positively influence hypertension by modulating the nervous system, immune system, and improving metabolic function. This review aims to elucidate the complex interactions among exercise training, gut microbiota, and hypertension.

Objective: To introduce bilateral hypertensive retinopathy (HR) (grade 4) complicated with macular edema (ME) patients with binocular intravitreal injection of anti-vascular endothelial growth factor (anti-VEGF) treatment.

Methods: Three cases of hypertensive retinopathy were observed. The fundus examination was consistent with HR (grade 4). The patients received anti-VEGF intraocular injection.

Results: The patient's ME and optic nerve edema were significantly reduced, visual acuity was significantly improved, and a case of secondary choroidal neovascularization (CNV) in the fundus of HR (grade 4) was also noted.

Conclusions: The use of intravitreal anti-VEGF agents in stage IV hypertensive retinopathy appears satisfactory but not perfect. In severe cases with vitreous hemorrhage, early injection avoids vitrectomy.

Background: Circulating microRNA-210-3p (miR-210-3p) is a hypoxia-related regulator implicated in placental maladaptation. Its longitudinal behavior across hypertensive disorders of pregnancy (HDP), and whether low-dose aspirin modifies its trajectory, remain insufficiently understood.

Methods: This prospective case-control study was conducted between October 2021 and November 2024. Circulating miR-210-3p was measured in the first trimester and at delivery. Aspirin use followed routine clinical practice for preeclampsia prevention. Longitudinal trajectories were examined using generalized estimating equations (GEE) as the primary analytic approach and linear mixed effects models (LMM) as a secondary method.

Results: Ninety-four women were enrolled, including 73 controls, 11 with gestational hypertension, and 10 with preeclampsia. miR-210-3p increased significantly from the first trimester to delivery in gestational hypertension (p = 0.003) and preeclampsia (p = 0.006), with no significant change in controls. In the first trimester, gestational hypertension exceeded controls (p = 0.006), and preeclampsia exceeded both groups (both p < 0.001). At delivery, gestational hypertension and preeclampsia remained higher than controls (both p < 0.001), and preeclampsia exceeded gestational hypertension (p = 0.036). GEE demonstrated a significantly slower rise in miR-210-3p among aspirin users with gestational hypertension (p = 0.042), and this association strengthened in sensitivity analysis (p = 0.001). LMM showed a similar, non-significant trend.

Conclusion: miR-210-3p exhibited disorder-specific longitudinal patterns across HDP. Aspirin-associated changes were observed in gestational hypertension but not in preeclampsia, suggesting differences in molecular expression trajectories between the two conditions over the course of gestation, while the underlying biological mechanisms remain to be clarified.

Background: Alcoholic cardiomyopathy (ACM) is a major cause of cardiovascular morbidity and mortality, characterized by ventricular dilation and impaired contractility resulting from chronic heavy alcohol use. Understanding its temporal and demographic trends is vital for guiding targeted public health interventions.

Methods and findings: Using the Global Burden of Disease (GBD) 2019 dataset, we analyzed ACM trends from 1990 to 2019 across 204 countries and territories. Multi-level mixed-effects models were applied to assess age, period, and cohort effects on ACM mortality. Males consistently exhibited higher ACM rates across all age groups. Although global age-standardized prevalence and mortality rates have declined since 1990, regional disparities persist-mortality remains highest in Eastern Europe and lowest in Sub-Saharan Africa. Age, period, and cohort analyses revealed patterns reflecting cumulative alcohol-related cardiac damage, healthcare advancements, and generational shifts in alcohol consumption.

Conclusions: Despite global improvement, ACM continues to impose a substantial health burden. Early interventions and policies addressing alcohol use throughout the life course are essential. Future longitudinal studies should identify critical prevention windows and explore genetic and environmental interactions. Advances in precision medicine, big data, and artificial intelligence may further enhance personalized treatment and optimize global resource allocation against ACM.

Background: Malignant hypertension (mHTN) is a severe hypertensive emergency, often associated with renal deterioration. Kidney length may be of useful to identify patients with renal dysfunction. Whether kidney length in mHTN patients is associated with renal prognosis is unclear.

Methods: The study enrolled 280 mHTN patients with renal thrombotic microangiopathy (TMA) who underwent renal biopsy between 2008 and 2023. Linear regression was used to explore patient characteristics of kidney length. The association between kidney length and ≥15% increase in estimated glomerular filtration rate (eGFR), and end-stage renal disease (ESRD) was analyzed using Cox regression and logistic regression, respectively. Kidney length was analyzed in tertiles, using the first tertile as reference.

Results: Patients with larger kidney length had higher levels of body mass index (BMI) and eGFR, but lower levels of urea nitrogen, serum creatinine, uric acid, global sclerosis ratio, and tubular atrophy/interstitial fibrosis ratio. Kidney length was strongly positively correlated with BMI, and negatively related to tubular atrophy/interstitial fibrosis ratio. During the follow-up, 72 patients experienced a ≥15% increase in eGFR and 172 patients progressed to ESRD. Patients in the third tertile of kidney length had a better renal recovery outcome of ≥15% increase in eGFR and lower odds of ESRD.

Conclusions: In mHTN patients with renal TMA, large kidney length is associated with better renal function improvement of ≥15% increase in eGFR, and lower risk of ESRD. In clinical practice, the measurement of kidney length may serve as a non-invasive indicator to assess renal prognosis and inform timely treatment interventions in mHTN patients.

White-coat Uncontrolled Hypertension (WUH) is characterized by elevated office blood pressure but normal out-of-office levels, and it has shifted from a phenomenological concept to a precision diagnosis model centered on ambulatory and home monitoring. This study provides a comprehensive review of the evolution of definitions, epidemiology, pathophysiology, and risk evidence, and compares the diagnostic value of Office Blood Pressure Monitoring (OBPM), Ambulatory Blood Pressure Monitoring (ABPM), and Home Blood Pressure Monitoring (HBPM). Within this analytical framework, the investigation examines cardiovascular and metabolic risks, interventions in special populations, and ongoing controversies in treatment. These findings are significant for integrating both Chinese and international guidelines with emerging digital monitoring trends. The study further proposes an integrated "home-clinic-cloud platform" model to support individualized hypertension management. This framework offers a more nuanced understanding of evolving paradigms in hypertension diagnosis and treatment. Based on current guideline-supported evidence, we emphasize ABPM/HBPM-based confirmation, risk stratification, and long-term surveillance to avoid misclassification and overtreatment. Emerging directions-including psycho-physiological modeling, multi-scenario monitoring, and digital-twin-enabled simulation-should be regarded as conceptual or research-oriented frameworks that require prospective validation and outcome data before clinical implementation.

Introduction: Metabolic dysfunction-associated steatohepatitis (MASH) is characterized by disrupted hepatic lipid homeostasis and progressive liver injury, and frequently coexists with hypertension and systemic vascular remodeling, suggesting shared pathophysiological mechanisms. Although adipose tissue-derived microRNAs have emerged as important mediators of inter-organ communication, their roles in regulating hepatic cholesterol metabolism and vascular dysfunction during MASH remain incompletely understood.

Objectives: This study aimed to investigate whether microRNA-518a regulates hepatic cholesterol metabolism and MASH progression through the MST1-AMPK-SREBP2 signaling pathway and to explore its potential implications for vascular remodeling and hypertension.

Methods: Integrative bioinformatic analyses, including Mendelian randomization and transcriptomic network analysis, were performed to identify candidate regulatory pathways associated with MASH. Functional validation was conducted using human clinical samples, in vitro cell models, exosome-mediated microRNA delivery, and a dietary mouse model of MASH.

Results: MST1 was identified as a key regulatory target of microRNA-518a. Increased microRNA-518a expression suppressed MST1, resulting in reduced AMPK activation and enhanced SREBP2-mediated cholesterol biosynthesis. Functional experiments demonstrated that microRNA-518a promoted hepatic cholesterol accumulation, lipid deposition, inflammation, and fibrotic changes, whereas restoration of MST1 partially reversed these effects. Exosome-mediated delivery of microRNA-518a further supported its ability to modulate hepatic metabolic responses through intercellular communication.

Conclusions: MicroRNA-518a promotes hepatic cholesterol dysregulation and MASH progression by targeting the MST1-AMPK-SREBP2 signaling pathway. Notably, the convergence of this axis with vascular regulatory networks suggests broader implications for understanding the metabolic-vascular comorbidities frequently observed in MASH patients, including hypertension and arterial stiffness.

Introduction: PCOS is a common endocrine disorder with elevated cardiometabolic risk, yet the role of the renin-angiotensin system (RAS)-iron metabolism axis in this comorbidity remains unclear. We explored its underlying mechanisms and evaluated the therapeutic potential of gentiopicroside.

Methods: Integrated multi-omics analyses combining transcriptomics, single-cell RNA sequencing, Mendelian randomization, machine learning, molecular docking, and in vitro functional assays were performed to identify shared molecular pathways and therapeutic targets across PCOS, hypertension, NAFLD, and T2DM.

Results: SLC11A2 was consistently dysregulated in PCOS transcriptomic datasets, and associated with iron metabolism, inflammatory response and oxidative stress pathways. Genetic analyses validated RAS-related regulation in hypertension susceptibility and revealed shared genetic architecture between PCOS and cardiometabolic traits. Network and single-cell analyses characterized SLC11A2-associated molecular patterns in disease-relevant cell types; machine learning identified disease-classifying molecular signatures. Gentiopicroside alleviated inflammatory and oxidative stress phenotypes, including reduced IL-6 expression and reactive oxygen species accumulation.

Conclusion: This study defines an RAS-SLC11A2 molecular framework linking iron metabolism dysregulation to PCOS-related cardiometabolic risk, elucidating the mechanisms connecting ovarian dysfunction, inflammation, oxidative stress and hypertension, and supports gentiopicroside as a promising therapeutic candidate.

Heart failure (HF) is a complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood. Globally, the morbidity and mortality of HF are still on the rise, especially in elderly individuals, and the low 5-year survival rate of HF is a major social and health management problem. The pathogenesis of heart failure involves genetic factors and persistent cardiac inflammation. Genetic factors typically increase a patient's susceptibility to specific diseases. Notably, persistent cardiac inflammation is also a significant contributor to heart failure. Whether it is spontaneous aseptic inflammation of the heart or inflammation caused by infection, both can lead to excessive activation of the immune system, thereby triggering adverse cardiac remodeling. This review focuses on describing the inflammatory/immune activation mechanisms involved in heart failure and explores targeted drugs for inflammatory/immune activation. Additionally, we focused on the NLRP3 inflammasome (a cellular signaling protein complex), whose excessive activation produces large number of inflammatory factors, including IL-1β and IL-18, ultimately leading to persistent inflammation and excessive immune activation in the myocardium, which in turn triggers myocardial cell death and adverse remodeling. We have revealed the pathogenic role of NLRP3 in heart failure, providing a theoretical basis for further research into heart failure.