LncRNA PSR Regulates Vascular Remodeling Through Encoding a Novel Protein Arteridin.

Rationale: Vascular smooth muscle cells (VSMCs) phenotype switch from contractile to proliferative phenotype is a pathological hallmark in various cardiovascular diseases. Recently, a subset of long noncoding RNAs was identified to produce functional polypeptides. However, the functional impact and regulatory mechanisms of long noncoding RNAs in VSMCs phenotype switching remain to be fully elucidated.

GlycA, hsCRP differentially associated with MI, ischemic stroke: In the Dallas Heart Study and Multi-Ethnic Study of Atherosclerosis: GlycA, hsCRP Differentially Associated MI, Stroke.

Objective: Inflammatory markers are associated with cardiovascular disease (CVD); however, the ability to specifically predict myocardial infarction (MI) as well as ischemic stroke remains unknown. There has not been a direct comparison of the associations between GlycA and hsCRP and MI and ischemic stroke in a multi-ethnic pooled cohort.

Methods: Multi-center, multi-ethnic, population-based community prospective pooled cohort of the Dallas Heart Study (DHS) and Multi-Ethnic Study of Atherosclerosis (MESA).

Prenatal Lipopolysaccharides Exposure Induces Transgenerational Inheritance of Hypertension.

Background: Adverse environmental exposure during the prenatal period can lead to diseases in the offspring, including hypertension. Whether or not the hypertensive phenotype can be transgenerationally transmitted is not known.

Methods: Pregnant Sprague Dawley rats were intraperitoneally injected with lipopolysaccharide (LPS) on gestation days 6, 8, 10, and 12 to generate the prenatal LPS exposure model.

Association of T-box gene polymorphisms with the risk of Wolff-Parkinson-White syndrome in a Han Chinese population.

Abnormal development of the atrioventricular ring can lead to the formation of a bypass pathway and the occurrence of Wolff-Parkinson-White (WPW) syndrome. The genetic mechanism underlying the sporadic form of WPW syndrome remains unclear. Existing evidence suggests that both T-box transcription factor 3 (TBX3) and T-box transcription factor 2 (TBX2) genes participate in regulating annulus fibrosus formation and atrioventricular canal development.

Limb Ischemia Complications of Veno-Arterial Extracorporeal Membrane Oxygenation.

Background: This study aimed to summarize and analyse the risk factors, clinical features, as well as prevention and treatment of limb ischemia complications in patients on veno-arterial extracorporeal membrane oxygenation (V-A ECMO).

Methods: We retrospectively analyzed 179 adult patients who had undergone V-A ECMO support in the Cardiac Care Unit of the First Hospital of Lanzhou University between March 2019 and December 2021. Patients were divided into the limb ischemia group (LI group) and the non-limb ischemia group (nLI group) according to whether limb ischemia occurred on the ipsilateral side of femoral artery cannulation.

Inhibition of DYRK1A, via histone modification, promotes cardiomyocyte cell cycle activation and cardiac repair after myocardial infarction.

Background: While the adult mammalian heart undergoes only modest renewal through cardiomyocyte proliferation, boosting this process is considered a promising therapeutic strategy to repair cardiac injury. This study explored the role and mechanism of dual-specificity tyrosine regulated kinase 1A (DYRK1A) in regulating cardiomyocyte cell cycle activation and cardiac repair after myocardial infarction (MI).

Methods: DYRK1A-knockout mice and DYRK1A inhibitors were used to investigate the role of DYRK1A in cardiomyocyte cell cycle activation and cardiac repair following MI.

G-protein-coupled receptor kinase 4 causes renal angiotensin II type 2 receptor dysfunction by increasing its phosphorylation.

Activation of the angiotensin II type 2 receptor (AT2R) induces diuresis and natriuresis. Increased expression or/and activity of G-protein-coupled receptor kinase 4 (GRK4) or genetic variants (e.g.

Veno-Arterial Extracorporeal Membrane Oxygenation in Elective High-Risk Percutaneous Coronary Interventions.

Background: The safety and feasibility of veno-arterial extracorporeal membrane oxygenation (VA-ECMO) as mechanical circulatory support in high-risk percutaneous coronary intervention (HR-PCI) remain unclear.

Methods: This retrospective study included patients with complex and high-risk coronary artery disease who underwent elective PCI with VA-ECMO support pre-operatively during March 2019-December 2020. Rates of VA-ECMO-related complications, complications during PCI, death, myocardial infarction, and stroke during hospitalisation and 1-year post-operatively were analysed.

Rosmarinic Acid Ameliorates Pulmonary Ischemia/Reperfusion Injury by Activating the PI3K/Akt Signaling Pathway.

Pulmonary ischemia/reperfusion (IR) injury is the leading cause of acute lung injury, which is mainly attributed to reactive oxygen species (ROS) induced cell injuries and apoptosis. Since rosmarinic acid (RA) has been identified as an antioxidant natural ester, this natural compound might protect against pulmonary IR injury. In this study, the mice were given RA daily (50, 75, or 100 mg/kg) by gavage for 7 days before the pulmonary IR injury.

NLRP3 inflammasome contributes to endothelial dysfunction in angiotensin II-induced hypertension in mice.

Aims: Inflammation is a key feature of endothelial dysfunction induced by angiotensin (Ang) II. The purpose of this study was to explore the role of Nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome in endothelial dysfunction in Ang II-induced hypertension.

Materials And Methods: We analyzed blood pressure and vascular function of wild-type (WT) and Nlrp3 knockout (Nlrp3) mice, treated with Ang II.

LKB1 suppression promotes cardiomyocyte regeneration via LKB1-AMPK-YAP axis.

The regenerative potential of cardiomyocytes in adult mammals is limited. Previous studies reported that cardiomyocyte proliferation is suppressed by AMP-activated protein kinase (AMPK). The role of liver kinase B1 (LKB1), as the major upstream kinase for AMPK, on cardiomyocyte proliferation is unclear.

Development and Validation of Prediction Models for Hypertensive Nephropathy, the PANDORA Study.

Importance: Hypertension is a leading cause of end-stage renal disease (ESRD), but currently, those at risk are poorly identified.

Objective: To develop and validate a prediction model for the development of hypertensive nephropathy (HN).

Design Setting And Participants: Individual data of cohorts of hypertensive patients from Kailuan, China served to derive and validate a multivariable prediction model of HN from 12, 656 individuals enrolled from January 2006 to August 2007, with a median follow-up of 6.

Loss of NPPA-AS1 promotes heart regeneration by stabilizing SFPQ-NONO heteromer-induced DNA repair.

The role of long non-coding RNA (lncRNA) in endogenous cardiac regeneration remains largely elusive. The mammalian cardiomyocyte is capable of regeneration for a brief period after birth. This fact allows the exploration of the roles of critical lncRNAs in the regulation of cardiac regeneration.

Synergistic Effect of Uroguanylin and D Dopamine Receptors on Sodium Excretion in Hypertension.

Background Oral NaCl produces a greater natriuresis and diuresis than the intravenous infusion of the same amount of NaCl, indicating the existence of a gastro-renal axis. As one of the major natriuretic hormones secreted by both the intestines and the kidney, we hypothesized that renal uroguanylin interacts with dopamine receptors to increase sodium excretion synergistically, an impaired interaction of which may be involved in the pathogenesis of hypertension. Methods and Results In Wistar-Kyoto rats, the infusion of uroguanylin or fenoldopam (a D-like receptor agonist) induced natriuresis and diuresis.

Correlation between Renal Artery Anatomy and Hypertension: A Retrospective Analysis of 3000 Patients.

Objective: To assess the correlation between renal artery anatomy and blood pressure in Undiagnosed Hypertension and Diagnosed Hypertension.

Methods: The renal artery CT scanning imaging data and laboratory data of 3000 inpatients and outpatients were collected retrospectively in 4 centers of China. Morphometric parameters were assessed using the quantitative vascular analysis (unit: mM).

Circular RNA circEsyt2 regulates vascular smooth muscle cell remodeling via splicing regulation.

Circular RNAs (circRNAs) have been recently recognized as playing a role in the pathogenesis of vascular remodeling-related diseases by modulating the functions of miRNAs. However, the interplay between circRNAs and proteins during vascular remodeling remains poorly understood. Here, we investigated a previously identified circRNA, circEsyt2, whose expression is known to be upregulated during vascular remodeling.

LARP7 ameliorates cellular senescence and aging by allosterically enhancing SIRT1 deacetylase activity.

Cellular senescence is associated with pleiotropic physiopathological processes, including aging and age-related diseases. The persistent DNA damage is a major stress leading to senescence, but the underlying molecular link remains elusive. Here, we identify La Ribonucleoprotein 7 (LARP7), a 7SK RNA binding protein, as an aging antagonist.

Paternal long-term PM2.5 exposure causes hypertension via increased renal AT1R expression and function in male offspring.

Maternal exposure to fine particulate matter (PM2.5) causes hypertension in offspring. However, paternal contribution of PM2.

Cardiogenic Shock After Acute Myocardial Infarction: A Review.

Importance: Cardiogenic shock affects between 40 000 and 50 000 people in the US per year and is the leading cause of in-hospital mortality following acute myocardial infarction.

Observations: Thirty-day mortality for patients with cardiogenic shock due to myocardial infarction is approximately 40%, and 1-year mortality approaches 50%. Immediate revascularization of the infarct-related coronary artery remains the only treatment for cardiogenic shock associated with acute myocardial infarction supported by randomized clinical trials.

Membrane-delimited signaling and cytosolic action of MG53 preserve hepatocyte integrity during drug-induced liver injury.

Background & Aims: Drug-induced liver injury (DILI) remains challenging to treat and is still a leading cause of acute liver failure. MG53 is a muscle-derived tissue-repair protein that circulates in the bloodstream and whose physiological role in protection against DILI has not been examined.

Methods: Recombinant MG53 protein (rhMG53) was administered exogenously, using mice with deletion of Mg53 or Ripk3.

The Protective Role of Yin-Yang 1 in Cardiac Injury and Remodeling After Myocardial Infarction.

Background Exploring potential therapeutic target is of great significance for myocardial infarction (MI) and post-MI heart failure. Transcription factor Yin-Yang 1 (YY1) is an essential regulator of apoptosis and angiogenesis, but its role in MI is unclear. Methods and Results The expression of YY1 was assessed in the C57BL/6J mouse heart following MI.

Effects of SGLT-2 inhibitors on health-related quality of life and exercise capacity in heart failure patients with reduced ejection fraction: A systematic review and meta-analysis.

Objective: Improving health-related quality of life (HRQoL) and exercise capacity is an important goal of treatment in heart failure (HF). However, evidence for the effects of sodium-glucose cotransporter-2 (SGLT-2) inhibitors on the improvement of HRQoL and exercise capacity seems to be conflicted. We performed a systematic review and meta-analysis to evaluate the effects of SGLT-2 inhibitors on HRQL and exercise capacity in patients with heart failure and reduced ejection fraction (HFrEF).

The Emerging Role of Irisin in Cardiovascular Diseases.

Irisin, a novel hormone like polypeptide, is cleaved and secreted by an unknown protease from a membrane-spanning protein, FNDC5 (fibronectin type III domain-containing protein 5). The current knowledge on the biological functions of irisin includes browning white adipose tissue, regulating insulin use, and anti-inflammatory and antioxidative properties. Dysfunction of irisin has shown to be involved in cardiovascular diseases such as hypertension, coronary artery disease, myocardial infarction, and myocardial ischemia-reperfusion injury.