The Association between Aortic Valve Stenosis and a Subsequent Diagnosis of Depression in Germany.

: Aortic valve stenosis (AS) represents one of the most common valve diseases in the western world. It often leads to severe symptoms that can lead to a restriction of everyday life and thus to psychological stress. Therefore, we aimed to investigate the association between AS and depression in outpatients in Germany.

Loss of ceramide synthase 5 inhibits the development of experimentally induced aortic valve stenosis.

Aim: Inflammation and calcification are hallmarks in the development of aortic valve stenosis (AVS). Ceramides mediate inflammation and calcification in the vascular tissue. The highly abundant d18:1,16:0 ceramide (C16) has been linked to increased cardiovascular mortality and obesity.

Cholesterol Crystal Dissolution Rate of Serum Predicts Outcomes in Patients With Aortic Stenosis Undergoing Transcatheter Aortic Valve Replacement.

Background: Aortic stenosis has pathophysiological similarities with atherosclerosis, including the deposition of cholesterol-containing lipoproteins. The resulting cholesterol crystals activate the NLRP3 (NOD-like receptor protein 3) inflammasome, leading to inflammation and cardiovascular diseases. We aimed to investigate the cholesterol crystal dissolution rate (CCDR) of serum in patients with aortic stenosis and to assess the prognostic value of this biomarker.

Toll-like receptor-3 contributes to the development of aortic valve stenosis.

Aortic valve stenosis (AS) development is driven by distinct molecular and cellular mechanisms which include inflammatory pathways. Toll-like-receptor-3 (TLR3) is a lysosomal pattern-recognition receptor that binds double-stranded RNA and promotes pro-inflammatory cellular responses. In recent years, TLR3 has emerged as a major regulator of vascular inflammation.

Circulating MicroRNA-122-5p Is Associated With a Lack of Improvement in Left Ventricular Function After Transcatheter Aortic Valve Replacement and Regulates Viability of Cardiomyocytes Through Extracellular Vesicles.

Background: Transcatheter aortic valve replacement (TAVR) is a well-established treatment option for high- and intermediate-risk patients with severe symptomatic aortic valve stenosis. A majority of patients exhibit improvements in left ventricular ejection fraction (LVEF) after TAVR in response to TAVR-associated afterload reduction. However, a specific role for circulating microRNAs (miRNAs) in the improvement of cardiac function for patients after TAVR has not yet been investigated.

CX3CR1 is a prerequisite for the development of cardiac hypertrophy and left ventricular dysfunction in mice upon transverse aortic constriction.

The CX3CL1/CX3CR1 axis mediates recruitment and extravasation of CX3CR1-expressing subsets of leukocytes and plays a pivotal role in the inflammation-driven pathology of cardiovascular disease. The cardiac immune response differs depending on the underlying causes. This suggests that for the development of successful immunomodulatory therapy in heart failure due to chronic pressure overload induced left ventricular (LV) hypertrophy, the underlying immune patterns must be examined.

AIM2 Stimulation Impairs Reendothelialization and Promotes the Development of Atherosclerosis in Mice.

Atherosclerosis has been shown to result from chronic inflammation caused by constitutive activation of the pattern recognition receptors (PRR), which are principle effectors of the innate immune system. PRR are present in the endosome or on the cellular membrane and can sense the aberrant release of nucleic acids, which is often a sign of acute or chronic cellular damage. Absent in melanoma 2 (AIM2) is a PRR that is expressed by vascular cells and specializes in detecting cytoplasmic double-stranded DNA (dsDNA).

MicroRNA-mediated vascular intercellular communication is altered in chronic kidney disease.

Aims: Chronic kidney disease (CKD) is an independent risk factor for the development of coronary artery disease (CAD). For both, CKD and CAD, the intercellular transfer of microRNAs (miRs) through extracellular vesicles (EVs) is an important factor of disease development. Whether the combination of CAD and CKD affects endothelial function through cellular crosstalk of EV-incorporated miRs is still unknown.

Aortic Valve Stenosis: From Basic Mechanisms to Novel Therapeutic Targets.

Aortic valve stenosis is the most prevalent heart valve disease worldwide. Although interventional treatment options have rapidly improved in recent years, symptomatic aortic valve stenosis is still associated with high morbidity and mortality. Calcific aortic valve stenosis is characterized by a progressive fibro-calcific remodeling and thickening of the aortic valve cusps, which subsequently leads to valve obstruction.

Murine sca1/flk1-positive cells are not endothelial progenitor cells, but B2 lymphocytes.

Circulating sca1/flk1 cells are hypothesized to be endothelial progenitor cells (EPCs) in mice that contribute to atheroprotection by replacing dysfunctional endothelial cells. Decreased numbers of circulating sca1/flk1 cells correlate with increased atherosclerotic lesions and impaired reendothelialization upon electric injury of the common carotid artery. However, legitimate doubts remain about the identity of the putative EPCs and their contribution to endothelial restoration.

Sodium thiocyanate treatment attenuates atherosclerotic plaque formation and improves endothelial regeneration in mice.

Introduction: Atherosclerotic plaque formation is an inflammatory process that involves the recruitment of neutrophil granulocytes and the generation of reactive oxygen species (ROS). ROS formation by myeloperoxidase, a key enzyme in H2O2 degradation, can be modulated by addition of sodium thiocyanate (NaSCN). However, the therapeutic use of NaSCN to counteract atherogenesis has been controversial, because MPO oxidizes NaSCN to hypothiocyanous acid, which is a reactive oxygen species itself.

Graded murine wire-induced aortic valve stenosis model mimics human functional and morphological disease phenotype.

Aortic valve stenosis (AS) is the most common valve disease requiring therapeutic intervention. Even though the incidence of AS has been continuously rising and AS is associated with significant morbidity and mortality, to date, no medical treatments have been identified that can modify disease progression. This unmet medical need is likely attributed to an incomplete understanding of the molecular mechanism driving disease development.

Aging-Associated TNF Production Primes Inflammasome Activation and NLRP3-Related Metabolic Disturbances.

Accumulating evidence suggests that the activation of the innate branch of the immune system plays a pivotal role in the induction and perpetuation of metabolic and aging-related diseases. In this context, the NLRP3 inflammasome pathway has been identified as an important driver of sterile inflammatory processes. De novo protein synthesis of NLRP3 induced by signals such as TLR ligands or TNF is a prerequisite for sustained NLRP3 mediated caspase-1 cleavage and inflammasome activation.