Transcriptomics and proteomics revealed sex differences in human pulmonary microvascular endothelial cells.

Marked sexual dimorphism is displayed in the onset and progression of pulmonary hypertension (PH). Females more commonly develop pulmonary arterial hypertension, yet females with pulmonary arterial hypertension and other types of PH have better survival than males. Pulmonary microvascular endothelial cells play a crucial role in pulmonary vascular remodeling and increased pulmonary vascular resistance in PH.

High-Soluble-Fiber Diet Attenuates Hypoxia-Induced Vascular Remodeling and the Development of Hypoxic Pulmonary Hypertension.

Background: Hypoxic pulmonary hypertension is a difficult disease to manage that is characterized by sustained elevation of pulmonary vascular resistance and pulmonary artery pressure due to vasoconstriction, perivascular inflammation, and vascular remodeling. Consumption of soluble-fiber is associated with lower systemic blood pressure, but little is known about its ability to affect the pulmonary circulation.

Methods: Mice were fed either a low- or high-soluble-fiber diet (0% or 16.

Shear Stress Markedly Alters the Proteomic Response to Hypoxia in Human Pulmonary Endothelial Cells.

Blood flow produces shear stress that homeostatically regulates the phenotype of pulmonary endothelial cells, exerting antiinflammatory and antithrombotic actions and maintaining normal barrier function. Hypoxia due to diseases, such as chronic obstructive pulmonary disease (COPD), causes vasoconstriction, increased vascular resistance, and pulmonary hypertension. Hypoxia-induced changes in endothelial function play a central role in the development of pulmonary hypertension.

The role of diet-derived short-chain fatty acids in regulating cardiac pressure overload.

Heart failure (HF) is one of the leading causes of mortality and morbidity in the modern world whose increasing prevalence is associated with "Western" diet and sedentary lifestyles. Of particular concern is the increasing burden of HF with preserved ejection fraction (HFpEF) that involves complex pathophysiology and is difficult to treat. Pressure overload caused by hypertension (HTN) is the predominant driver of cardiac injury, left ventricular hypertrophy, and fibrosis that progresses to diastolic dysfunction and ultimately HFpEF.

Negative inotropic effects of diadenosine tetraphosphate are mediated by protein kinase C and phosphodiesterases stimulation in the rat heart.

Extracellular diadenosine polyphosphates (ApA) are recently considered as an endogenous signaling compounds with transmitter-like activity which present in numerous tissues, including heart. It has been demonstrated previously that extracellular ApA cause alteration of the heart functioning via purine receptors in different mammalian species. Nevertheless, principal intracellular pathways which underlie ApA action in the heart remain unknown.