Association between adequate dietary protein and all-cause and cardiovascular mortality in patients with selective glomerular hypofiltration syndrome.

Aims: To determine the impact of dietary protein intake and protein sources on all-cause and cardiovascular mortality of selective glomerular hypofiltration syndrome (SGHS) patients. Methods: This study recruited participants from the National Health and Nutrition Examination Survey (NHANES) conducted between 1999 and 2004. Cox proportional hazard models and competing risk models were employed to investigate the effects of dietary protein intake and protein sources on all-cause and cardiovascular mortality in SGHS patients. Additionally, Cox regression models utilizing restricted cubic splines (RCS) were used to explore potential non-linear associations. Results: Over a median follow-up period of 204 months, 20.71% (449/2168) participants died, with 5.40% (117/2168) experiencing cardiovascular mortality. In the fully adjusted model, participants with the highest dietary protein intake (Q4, ≥107.13 g d-1) exhibited a 40% reduced risk of all-cause mortality (HR: 0.60, 95% CI: 0.39 to 0.94) and an 88% reduced risk of cardiovascular mortality (HR: 0.12, 95% CI: 0.04 to 0.35) compared to those with the lowest dietary protein intake (Q1, < 57.93 g d-1). Notably, non-red meat protein sources were found to reduce the risk of all-cause and cardiovascular mortality, whereas no significant association was observed with red meat consumption. Conclusion: Adequate dietary protein intake has been linked to a decreased risk of all-cause and cardiovascular mortality in individuals with selective glomerular hypofiltration syndromes. This protective effect seems to be primarily associated with protein obtained from non-red meat sources.

Effect of tanshinone IIA for myocardial ischemia/reperfusion injury in animal model: preclinical evidence and possible mechanisms.

Introduction: Tanshinone IIA (Tan IIA), the major active lipophilic ingredient of Radix Salviae Miltiorrhizae, exerts various therapeutic effects on the cardiovascular system. We aimed to identify the preclinical evidence and possible mechanisms of Tan IIA as a cardioprotective agent in the treatment of myocardial ischemia/reperfusion injury. Methods: The study quality scores of twenty-eight eligible studies and data analyses were separately assessed using the CAMARADES 10-item checklist and Rev-Man 5.3 software. Results: The study quality score ranged from 3/10 to 7/10 points. The present study provided preliminary preclinical evidence that Tan IIA could significantly decrease the myocardial infarct size, cardiac enzyme activity and troponin levels compared with those in the control group (p < 0.05). Discussion: Tan IIA alleviated myocardial I/R injury via antioxidant, anti-inflammatory, anti-apoptosis mechanisms and improved circulation and energy metabolism. Thus, Tan IIA is a promising cardioprotective agent for the treatment of myocardial ischemia/reperfusion injury and should be further investigated in clinical trials.

circFAT1(e2) Inhibits Cell Apoptosis and Facilitates Progression in Vascular Smooth Muscle Cells through miR-298/MYB Axis.

Presently, as one of the three types of muscles in the human body, smooth muscle carries out many biological activities. Meanwhile, its abnormal development also leads to many diseases. Circular RNA, belonging to the noncoding RNA family, is demonstrated to function importantly in various diseases including smooth muscle. Here, we assumed circFAT1(e2) probably exhibited a primary role in vascular smooth muscle. Therefore, we conducted cell viability and cell apoptosis assay to validate the effects of circFAT1(e2) on vascular smooth muscle progression. Then, we supposed miR-298 was one target of circFAT1(e2) and executed corresponding experiments to test this hypothesis. Dual-luciferase reporter assay indicated miR-298 could bind to circFAT1(e2) and then modulated MYB level, thus regulating smooth muscle progression. Subsequently, based on the GSE41177 dataset, we identified 1982 differentially expressed genes (DEGs) in atrial fibrillation, and all DEGs were upregulated, including MYB. Finally, enrichment analysis of upregulated genes indicated that they were related to endodermal cell differentiation. The protein-protein interaction network revealed that EGFR, GNG2, and FPR2 were related to atrial fibrillation. In conclusion, our data find that circFAT1(e2) sponges miR-298 and then regulates MYB expression, thus affecting atrial fibrillation progression. Our findings provide a newly produced indicator and target for vascular smooth muscle diagnosis and treatment.

Sodium Selenite Attenuates Balloon Injury-Induced and Monocrotaline-Induced Vascular Remodeling in Rats.

Vascular remodeling (VR), induced by the massive proliferation and reduced apoptosis of vascular smooth muscle cells (VSMCs), is primarily responsible for many cardiovascular conditions, such as restenosis and pulmonary arterial hypertension. Sodium selenite (SSE) is an inorganic selenium, which can block proliferation and stimulate apoptosis of tumor cells; still, its protective effects on VR remains unknown. In this study, we established rat models with carotid artery balloon injury and monocrotaline induced pulmonary arterial hypertension and administered them SSE (0.25, 0.5, or 1 mg/kg/day) orally by feeding tube for 14 consecutive days. We found that SSE treatment greatly ameliorated the development of VR as evidenced by an improvement of its characteristic features, including elevation of the ratio of carotid artery intimal area to medial area, right ventricular hypertrophy, pulmonary arterial wall hypertrophy and right ventricular systolic pressure. Furthermore, PCNA and TUNEL staining of the arteries showed that SSE suppressed proliferation and enhanced apoptosis of VSMCs in both models. Compared with the untreated VR rats, lower expression of PCNA and CyclinD1, but higher levels of Cleaved Caspase-3 and Bax/Bcl-2 were observed in the SSE-treated rats. Moreover, the increased protein expression of MMP2, MMP9, p-AKT, p-ERK, p-GSK3ß and ß-catenin that occurred in the VR rats were significantly inhibited by SSE. Collectively, treatment with SSE remarkably attenuates the pathogenesis of VR, and this protection may be associated with the inhibition of AKT and ERK signaling and prevention of VSMC's dysfunction. Our study suggest that SSE is a potential agent for treatment of VR-related diseases.

Cerebral microbleeds are associated with blood pressure levels in individuals with hypertension.

Objective: Cerebral microbleeds (CMBs), which appear as small dot-like hypointense lesions, are strongly associated with cerebrovascular disease. Recently, numerous investigations have suggested that hypertension and age are risk factors for CMBs; however, whether blood pressure grade and age rank are related to the severity of CMBs remains unclear. The purpose of this research was to assess the association between cerebral microbleeds and blood pressure levels.Methods: In total, 460 consecutive hypertension patients (214 males and 246 females; aged 44-96 years, mean age 60.95 ± 6.82 years) from Lishui Central Hospital were enrolled and classified as CMB or non-CMB patients according to magnetic resonance imaging (MRI). Gradient echo T2*-weighted MRI was used to detect CMBs. Differences in blood pressure, CMB severity, and other patient characteristics were compared between the two groups. Multifactorial logistic regression was used to analyze the correlation between blood pressure and microbleeds.Results: In our study, CMB lesions were identified in 123 patients (26.7%), including 39 patients with CMB lesions located deep in the brain. In the hypertensive population, smoking is an independent risk factor for CMBs. Additionally, systolic blood pressure (SBP), diastolic blood pressure (DBP) and age are also independent risk factors for CMBs. Furthermore, a modest correlation was noted between the number of microbleeds and grade of hypertension.Conclusions: This study provides novel evidence that microbleed severity is associated with hypertension grade. This conclusion emphasizes the importance of antihypertensive therapy in hypertension patients to avoid an increase in CMBs.

Thymoquinone attenuates monocrotaline-induced pulmonary artery hypertension via inhibiting pulmonary arterial remodeling in rats.

BACKGROUND: Pulmonary artery remodeling induced by excess proliferation, migration and apoptosis resistance of pulmonary arterial smooth muscle cells (PASMCs) is a key component in pulmonary artery hypertension (PAH). Thymoquinone (TQ) triggers cancer cells apoptosis through multiple mechanisms. In addition, TQ inhibits migration of human nonsmall-cell lung cancer cells and human glioblastoma cells. OBJECTIVES: In the current study, we investigated effects of TQ on MCT-induced PAH in rats and its underlying mechanisms. METHODS: After 2weeks of monocrotaline injection (MCT, 60mg/kg), Male Sprague-Dawley rats received TQ (8mg/kg, 12mg/kg, 16mg/kg) or olive oil per day for 2weeks. Hemodynamic changes, right ventricular hypertrophy, and lung morphological features were examined 4weeks later. In addition, TUNEL, PCNA, α-SMA, Bax and Bcl-2 were detected by immunohistochemistry staining. Bax, Bcl-2, cleaved caspase-3, cleaved poly (ADP-ribose) polymerase (PARP) MMP2, MMP9 and activation of p38MAPK and NF-κB were assessed by Western blot. RESULTS: MCT-induced an increase in pulmonary blood pressure and right ventricular hypertrophy, which were attenuated by TQ treatment. TQ also blocked MCT-induced pulmonary arterial remodeling, proliferation of PASMCs, elevation of MMP2 and downregulation of ratio of Bax/Bcl-2, cleaved caspase-3 and cleaved PARP. Furthermore, TQ inhibited MCT-induced activation of p38MAPK and NF-κB. CONCLUSIONS: TQ ameliorates MCT-induced pulmonary artery hypertension by inhibiting pulmonary arterial remodeling partially via p38MAPK/NF-κB signaling pathway in rats.

Right coronary artery dissection and aneurysm presented as acute inferior myocardial infarction from an automobile airbag trauma.

Coronary artery dissection and aneurysm culminating in acute myocardial infarction are rare after blunt chest trauma. We are reporting a case of a previously healthy 52-year-old man who presented with right inferior lobe contusion, pleural effusion, right interlobar fissure effusion, bone fracture of right fourth rib, and acute inferior wall myocardial infarction and who experienced blunt trauma in his right chest wall by an airbag deployment in a car accident. Coronary angiography showed an aneurysm in the middle of right coronary artery with 70% afferent narrowing just distal to the aneurysm with no visible atherosclerotic lesion. A 4.0×20 mm TEXUS Liberté stent in the lesion was deployed, and a good coronary flow was obtained without residual stenosis and the aneurysm vanished.