Suppressed nuclear envelope proteins activate autophagy of vascular smooth muscle cells during cyclic stretch application.

Dysfunctions of vascular smooth muscle cells (VSMCs) play crucial roles in vascular remodeling in hypertension, which correlates with pathologically elevated cyclic stretch due to increased arterial pressure. Recent researches reported that autophagy, a life-sustaining process, was increased in hypertension. However, the mechanobiological mechanism of VSMC autophagy and its potential roles in vascular remodeling are still unclear.

Lamin A/C negatively regulated by miR-124-3p modulates apoptosis of vascular smooth muscle cells during cyclic stretch application in rats.

Aim: Apoptosis of vascular smooth muscle cells (VSMCs) influenced by abnormal cyclic stretch is crucial for vascular remodelling during hypertension. Lamin A/C, a nuclear envelope protein, is mechano-responsive, but the role of lamin A/C in VSMC apoptosis is still unclear.

Methods: FX-5000T Strain Unit provided cyclic stretch (CS) in vitro.

Single-cell analyses reveal functional classification of dendritic cells and their potential roles in inflammatory disease.

Dendritic cells (DCs) have crucial roles in immune-related diseases. However, it is difficult to explore DCs because of their rareness and heterogeneity. Although previous studies had been performed to detect the phenotypic characteristics of DC populations, the functional diversity has been ignored.

Cyclic stretch induces VEGFA alternative splicing via Serine/Arginine-Rich Splicing Factor 1.

Abnormal proliferation of vascular smooth muscle cells (VSMCs) induced by high cyclic stretch is crucial in the vascular remodeling during hypertension. Vascular endothelial growth factor A (VEGFA) alternative splicing plays important roles in the pathological process of vascular diseases and remodeling. However, the roles of VEGFA isoforms in modulating VSMC functions in response to cyclic stretch remain unclear.

Platelet-derived microparticles promote endothelial cell proliferation in hypertension via miR-142-3p.

Endothelial cells (ECs) are located at the interface between flowing blood and the vessel wall, and abnormal EC proliferation induced by pathologic environments plays an important role in vascular remodeling in hypertensive conditions. Exchanges of information between blood components and ECs are important for EC function. Hence, the present study sought to determine how platelets induce EC dysfunction under hypertensive conditions.

Atrial fibrillation: rhythm control offers no advantage over rate control for some, but not all.

Atrial fibrillation (AF) is not a benign condition. Although AF is the most common sustained cardiac arrhythmia, the management of AF remains controversial. In recent years, several clinical trials comparing rhythm control with rate control for AF management found that rhythm control offers no advantage over rate control, but the findings may not apply equally to all patients.