Endovascular repair has become state of the art for treating thoracic and abdominal aortic aneurysms. However, complications such as endoleaks or the development of aortic neck dilatation, require lifelong surveillance and re-interventions. The extent to which structural vessel wall alterations during implantation of endovascular grafts are involved in the development of these complications is widely unknown. Therefore, the aim of this study was to characterize aortic vessel wall alterations during endovascular aortic repair in a porcine ex-vivo model.

A total of 18 endovascular stent-grafts were implanted in a thoracoabdominal porcine aortic flow model. Subsequently, histomorphological analysis, transmission electron microscopy and biomechanical analysis of the proximal sealing zone was performed.

While histological wall impairment was detected in only four specimens (22%), transmission electron microscopy revealed ultrastructural disruption in all specimens after EVAR. Transmission electron microscopy revealed a disrupted structure of elastic fibers with microtears and cavities supplemented by ruptured collagen fibers and disrupted integrity of vascular smooth muscle cells in all aortic specimens after stent-graft implantation. As a biomechanical correlate to ultrastructural aortic wall injuries, a significantly lower force at rupture (55.63±14.71 vs. 36.56±12.27 N, P=0.006) and elongation at rupture (22.23±5.39 vs. 17.13±5.34 mm, P=0.048) were observed in aortic specimens after stent-graft implantation.

Endovascular stent-graft implantation induces acute ultrastructural damage to the aortic wall, including elastic fiber disintegration, collagen disruption, and microdissections within the tunica media. These alterations were associated with reduced biomechanical stability. Whether this initial mechanical injury contributes to long-term complications such as aortic neck dilatation warrants further investigation.

Patients with familial hypercholesterolemia (FH) are at high risk of coronary artery disease (CAD), and its prediction is of great clinical importance. This study aimed to identify predictors of CAD and construct an effective risk prediction model for Korean patients with FH.

Clinical and laboratory data of 245 patients were collected from the Korean FH registry. CAD was defined as ≥50% coronary stenosis on invasive or computed tomographic angiography. The cholesterol efflux capacity (CEC) was measured using J774A1 cells and radiolabeled cholesterol. Predictors of CAD were identified by multivariable logistic regression analysis, and the best-performing prediction model was determined based on its statistical indices.

The participants' mean age was 49.1 years; 92 (37.6%) were male, and 41 (16.7%) had CAD. Age [odds ratio (OR) 1.05; p=0.02], hypertension (OR 7.28; p<0.0001), low-density lipoprotein-cholesterol (OR 1.60; p=0.02), and high-density lipoprotein-cholesterol (HDL-C) (OR 0.93; p=0.002) were identified as predictors of CAD in the multivariable analysis. In another analysis, age, hypertension, body mass index (OR 1.16; p=0.03), and apolipoprotein A1 (OR 0.97; p=0.002) were predictive of CAD. CEC did not have a significant predictive value. The best-performing CAD prediction model included six clinical and laboratory variables, with an area under the curve of 0.878. The effects of hypertension, smoking, and HDL-C were particularly influential.

Traditional risk factors, including hypertension and HDL-C, were predictors of CAD in Korean patients with FH, whereas CEC was not. The resulting CAD prediction model demonstrated satisfactory performance in this population.

To observe the effect of acupuncture of "twelve hand and foot acupoints" (in fact "12 acupoints on the hands and feet") combined with neural mobilization intervention (a manual treatment method that directly applies force to some related nerve tissue through the placement and movement of multiple joints) on the limb motor function and quality of life in patients with cerebral infarction (CI) hemiplegia of qi-deficiency and blood-stasis type.

Ninety-eight patients with CI hemiplegia of qi-deficiency and blood-stasis type were randomly divided into a neural mobilization group (49 cases, 2 cases dropped out) and a combination (acupuncture plus neural mobilization) group (49 cases, 3 cases dropped out) using a random number table method. All patients underwent basic treatment and rehabilitation training, and those of the neural mobilization group received various manipulations at different portions of the body related to the innervation of radial nerve, median nerve, ulnar nerve, sciatic nerve, common peroneal nerve, tibial nerve and femoral nerve through the placement and movement of multiple joints. The patients of the combination group received manual acupuncture stimulation of 12 acupoints (including bilateral Neiguan [PC6], Hegu [LI4], Quchi [LI11], Yanglingquan [GB34], Zusanli [ST36] and Sanyinjiao [SP6], with the acupuncture needles retained for 30 min in every session of treatment) on the basis of the neural mobilization. The treatment was conducted once daily, 5 d a week for 4 weeks. The degree of neurologic impairment was assessed by China stroke scale (CSS). The score of qi-deficiency and blood-stasis syndrome was given according to "quantitative scoring scale for qi-deficiency and blood-stasis syndrome". The limb motor function was assessed using Fugl-Meyer assessment scale (FMA). The blood plasma viscosity and fibrinogen level were detected using a blood rheology analyzer. The score of quality of life was assessed using the stroke-specific quality of life scale (SS-QOL).

After 4 weeks of treatment, the CSS score, the score of qi-deficiency and blood-stasis syndrome, plasma viscosity and fibrinogen level were significantly lower in both groups than those pre-treatment (P<0.05), with the combination group showing obviously lower values than the neural mobilization group (P<0.05). The FMA score and SS-QOL score were considerably increased in both groups compared with those pre-treatment (P<0.05), and were strikingly higher in the combination group than in the neural mobilization group (P<0.05).

Acupuncture of "twelve hand and foot acupoints" combined with neural mobilization can effectively regulate blood rheology, improve symptoms and limb motor function, and raise the quality of life in patients with hemiplegia of qi-deficiency and blood-stasis type.

Based on the vessel-collateral theory, "qi deficiency and blood stasis leading to collateral obstruction and accumulation", electroacupuncture was delivered in patients with ventricular remodeling after percutaneous coronary intervention (PCI) for acute ST-segment elevation myocardial infarction (STEMI), and the clinical efficacy was evaluated.

A prospective randomized controlled design was adopted. Eighty patients with cardiac insufficiency after STEMI-PCI (qi deficiency and blood stasis) were enrolled and randomly assigned to a control group (40 cases, with 2 cases dropped out) and an electroacupuncture group (40 cases, with 2 cases dropped out). In the control group, the standardized western medication was administered. In the electroacupuncture group, on the basis of the regimen as the control group, electroacupuncture was operated at Neiguan (PC6), Danzhong (CV17), Shenmen (HT7), Qihai (CV6), Xuehai (SP10) and Zusanli (ST36) with dense-disperse wave, at a frequency of 2 Hz/100 Hz, 30 min per session, once every other day, for 8 consecutive weeks. Three-dimensional speckle tracking echocardiography was used to detect cardiac function indicators:left ventricular ejection fraction (LVEF) and global longitudinal strain (GLS), and cardiac structural indicators:left ventricular end-diastolic volume (LVEDV) and left ventricular end-systolic volume (LVESV) in both groups before and after treatment. ELISA was used to detect the serum levels of cardiac fibrosis markers:soluble suppression of tumorigenicity 2 (sST2) and galectin-3 (Gal-3);immunoturbidimetry was used to detect the heart failure marker:N-terminal pro-B-type natriuretic peptide (NT-proBNP). Changes in traditional Chinese medicine (TCM) syndrome scores were compared and the safety was evaluated in the two groups.

Compared with the control group, the electroacupuncture group showed the increase in LVEF and absolute value of GLS (P<0.01, P<0.001) and the decrease in LVEDV and LVESV (P<0.01, P<0.001) after treatment;serum fibrosis markers (sST2, Gal-3) levels were reduced (P<0.05, P<0.01), the serum heart failure marker (NT-proBNP) level was decreased (P<0.001), and the scores of TCM symptoms were improved (P<0.01, P<0.001). Gompared with before treatment, both groups showed improvement (P<0.001) in the above indicators after treatment. No serious adverse event was reported.

Electroacupuncture may conduce to ameliorating cardiac functions and ventricular remodeling indicators in patients after STEMI-PCI, which is probably related to the modulation of cardiac fibrosis markers in serum.

Cardiovascular disease (CVD) is the leading cause of death for women globally, and menopause is associated with elevated morbidity and mortality. The total impact of menopause on blood pressure remains inconclusive, with evidence largely based on data from industrialized populations. To address this gap, we examined associations between menopause, blood pressure, and hypertension among Tsimane forager-horticulturalists and compared results against a nationally representative US sample to assess population-level differences in blood pressure with menopause.

We analyzed data from female and male Tsimane (n_individuals = 5,570; n_observations = 18,676; ages 15-92) and US National Health and Nutrition Examination Survey participants (NHANES; n_individuals = 6,861; ages 16-80). We applied linear regression models to assess age and population effects on systolic (SBP) and diastolic blood pressure (DBP) with menopause, logistic regression models for hypertension and stage 2 hypertension, and mediation analyses with estradiol.

SBP age trajectories were higher (b = 0.002, p < 0.001) and DBP trajectories lower (b = -0.004, p < 0.001) following menopause. Compared to US women, Tsimane women's SBP increased more quickly with age (b = 0.001, p = 0.021), while DBP decreased less dramatically (b = 0.003, p < 0.001). Postmenopause individuals had lower odds of hypertension with age compared to premenopausal women. Estradiol did not mediate blood pressure effects of menopause.

We found similar associations between menopause and blood pressure in both populations, despite widely differing CVD risk environments. However, Tsimane women showed slightly different pressure changes with age postmenopause. These results indicate blood pressure change postmenopause may be universal, but premenopause CVD risk environments may impact postmenopause CVD risk outcomes.

Cardiometabolic diseases remain a major global health burden, and current therapies only partially address the persistent residual risk driven by chronic inflammation, hypoxia, metabolic overload, and mechanical stress. A critical need is to understand how these diverse stress signals are integrated at the cellular and molecular levels to determine whether tissues adapt or undergo pathological remodeling. This review presents a comprehensive framework of kinase-microRNA (miRNA) crosstalk as an emerging regulatory axis in cardiometabolic disease. We discuss how stress-activated kinase pathways, including ERK, p38/JNK, PI3K-Akt-mTOR/S6K2, AMPK, GSK-3, and EGFR, reprogram miRNA output through phosphorylation of key components of the miRNA machinery, including DROSHA/DGCR8, DICER-TRBP, and AGO2. These phosphorylation-dependent mechanisms influence miRNA processing, substrate selection, RISC assembly, and target repression in a context-dependent manner. We further highlight the reciprocal regulation whereby miRNAs modulate kinase signaling pathways, establishing feedback networks that regulate inflammation, apoptosis, fibrosis, angiogenesis, and metabolic adaptation across cardiac, vascular, and immune cells. Emerging technologies, including AGO2 eCLIP, phosphoproteomics, CRISPR-based perturbations, and single-cell/spatial profiling, allow causal mapping of kinase-miRNA networks. Collectively, these advances establish kinase-miRNA crosstalk as a promising mechanistic framework and therapeutic target for precision intervention in heart failure, atherosclerosis, diabetic cardiomyopathy, and related cardiometabolic diseases.

Uncontrolled and resistant hypertension continues to be a significant contributor to cardiovascular and renal risk. Baxdrostat is a selective aldosterone synthase inhibitor which has demonstrated a potential blood pressure-lowering effect in randomized controlled trials (RCTs). We performed a systematic literature search across PubMed, Scopus, Web of Science, and Cochrane from their inception to March 2026. The continuous outcomes were reported as mean differences (MDs), and dichotomous outcomes as relative risks (RRs), both with their corresponding 95% confidence intervals (CIs). In four RCTs involving 1481 participants, baxdrostat reduced mean sitting systolic and diastolic blood pressure significantly more than placebo (MD =  - 8.93 mmHg and MD =  - 3.79 mmHg, respectively), with no heterogeneity. Benefits were observed with both 1 mg and 2 mg daily doses. Baxdrostat was associated with a higher incidence of adverse events overall (RR = 1.24; 95% CI, 1.07 to 1.43), higher serum potassium levels (MD = 0.47 mmol per liter), and greater risks of hyperkalemia (RR = 8.64; 95% CI, 3.56 to 20.98) and potassium levels of more than 6 mmol per liter (RR = 6.06; 95% CI, 1.66 to 22.17), whereas serious adverse events were not significantly increased. In patients having uncontrolled or resistant hypertension, baxdrostat reduced sitting systolic and diastolic blood pressure compared to placebo. These results are based on a few RCTs, and the increased risk of hyperkalemia warrants caution. Further studies are required to provide enlightenment on long-term safety and general clinical benefit.

This study aims to estimate the effects of vitamin D supplementation on cardiovascular diseases in populations with different baseline vitamin D distributions, by emulating the VITAL and D-Health trials within the UK Biobank. We emulated randomized trials using subcohorts of the UK Biobank selected to match the inclusion criteria of the VITAL and D-Health trials (n = 237,502 and 185,809, respectively). Exposures were defined as increases in serum 25-hydroxyvitamin-D concentrations of 30 nmol/L and 38 nmol/L, corresponding to the intervention effects in the trials. Outcomes included cardiovascular mortality, myocardial infarction, ischemic stroke, and major adverse cardiovascular events. Expected hazard ratios over trial median follow-up durations of 5.3 and 5.7 years were estimated using Cox proportional hazards models. Vitamin D insufficiency was more common in the UK Biobank than in the original trials. When participants were weighted to match the trial baseline 25-hydroxyvitamin-D distributions, the expected effects became more similar to the largely null findings reported in the original trials. By contrast, among individuals with vitamin D insufficiency or deficiency, increases in 25-hydroxyvitamin-D concentration as achieved in the trials were associated with significantly lower risks of cardiovascular outcomes, except ischemic stroke. For cardiovascular mortality, hazard ratios ranged from 0.74 (95% CI 0.62-0.88) to 0.79 (95% CI 0.69-0.91) across both trial emulations. The largely null findings observed in the trials may partly reflect that the trial populations were predominantly vitamin D-replete. Our emulated trials suggest that substantial cardiovascular benefits from vitamin D supplementation may be expected among populations with low vitamin D status.

TMEM16A forms a Ca²⁺-activated Cl⁻ channel in vascular mural cells (smooth muscle cells and pericytes) that generates depolarizing Cl⁻ efflux upon intracellular Ca²⁺ elevation, thereby amplifying agonist-induced vasoconstriction. TMEM16A has been implicated in excessive capillary pericyte constriction following cerebral ischemia, suggesting that its inhibition may improve post-stroke recovery. However, the impact of systemic vascular TMEM16A inhibition on focal reperfusion efficiency and cerebrovascular autoregulation remains unknown. To address this question, mice with inducible mural cell-specific (Myosin Heavy Chain 11 promoter controlled) deletion of TMEM16A were subjected to transient middle cerebral artery occlusion. Reperfusion dynamics and stroke-reperfusion outcome were assessed using laser speckle contrast imaging, cylinder test for motor function, and infarct quantification by 2,3,5-triphenyltetrazolium chloride staining. Systemic cardiovascular parameters were monitored with radiotelemetry. Middle cerebral artery myogenic tone was assessed with pressure myography. Mice lacking TMEM16A in mural cells exhibited impaired reperfusion and worsened stroke outcome compared with wild-type controls, despite unchanged systemic cardiovascular parameters. In wild-type mice, capillary pericytes maintained basal contractile tone in both hemispheres, and this was further enhanced in peri-infarct cortex. In contrast, TMEM16A-deficient capillary pericytes lacked basal tone in both the ipsilateral and contralateral hemispheres. TMEM16A-deficient middle cerebral arteries failed to develop pressure-induced myogenic tone. These findings demonstrate that TMEM16A is required for effective cerebral autoregulation and that its deficiency significantly impairs post-ischemic reperfusion. The results caution against systemic TMEM16A inhibition as a therapeutic strategy for stroke and highlight the need for spatially restricted approaches to modulate cerebral perfusion via the Ca²⁺-activated Cl⁻ channels.

Ehlers-Danlos syndrome (EDS) is a congenital connective tissue disorder that is often marked by chronic pain and considerable functional impairment. Pain in EDS is typically multifaceted, involving musculoskeletal, neuropathic, autonomic, and centralized pain components. The present investigation, therefore, aims to examine common pain phenotypes and mechanisms in EDS and to discuss strategies for interdisciplinary pain management briefly.

Recent studies have identified multiple sources of pain etiologies in EDS, including joint instability, repetitive microtrauma, small fiber neuropathy, and dysfunctional central pain processing. There is also growing evidence that nociceptive pain mechanisms and psychological factors may play a role in pain experience. Furthermore, current literature promotes multidisciplinary care models that synthesize physical therapy targeting joint stabilization and neuromuscular control, symptom-specific pharmacologic therapy, and psychological interventions. In addition, recent studies have investigated complementary therapies, including trigger-point injections, that may provide benefit. Despite this, high-quality evidence supporting interventional and specific pharmacologic regimens remains sparse. EDS pain remains multifaceted and requires an individualized and mechanism-informed approach to treatment. Integrated care models that include rehabilitation, phenotype-guided pharmacotherapy, and behavioral interventions form the bedrock of management. Ongoing research is necessary to refine phenotype-driven treatment strategies further.