Transcriptome studies of inherited dilated cardiomyopathies.

Dilated cardiomyopathy (DCM) is a group of heart muscle diseases that often lead to heart failure, with more than 50 causative genes have being linked to DCM. The heterogenous nature of the inherited DCMs suggest the need of precision medicine. Consistent with this emerging concept, transcriptome studies in human patients with DCM indicated distinct molecular signature for DCMs of different genetic etiology.

SIRT1 and Autophagy: Implications in Endocrine Disorders.

Autophagy is a cellular process involved in the selective degradation and recycling of dysfunctional intracellular components. It plays a crucial role in maintaining cellular homeostasis and survival by removing damaged and harmful proteins, lipids, and organelles. SIRT1, an NAD-dependent multifunctional enzyme, is a key regulator of the autophagy process.

Regulation of total LC3 levels by angiotensin II in vascular smooth muscle cells.

Hypertension is associated with high circulating angiotensin II (Ang II). We have reported that autophagy regulates Ang II-induced vascular smooth muscle cell (VSMC) hypertrophy, but the mechanism mediating this effect is still unknown. Therefore, we studied how Ang II regulates LC3 levels in VSMCs and whether Bag3, a co-chaperone known to regulate LC3 total levels, may be involved in the effects elicited by Ang II.

Hydrochlorothiazide Reduces Cardiac Hypertrophy, Fibrosis and Rho-Kinase Activation in DOCA-Salt Induced Hypertension.

Background: Thiazides are one of the most common antihypertensive drugs used for hypertension treatment and hydrochlorothiazide (HCTZ) is the most frequently used diuretic for hypertension treatment. The Rho/Rho-kinase (ROCK) path plays a key function in cardiovascular remodeling. We hypothesized that in preclinical hypertension HCTZ reduces myocardial ROCK activation and consequent myocardial remodeling.

Angiotensin II-Regulated Autophagy Is Required for Vascular Smooth Muscle Cell Hypertrophy.

Hypertension is a disease associated to increased plasma levels of angiotensin II (Ang II). Ang II can regulate proliferation, migration, ROS production and hypertrophy of vascular smooth muscle cells (VSMCs). However, the mechanisms by which Ang II can affect VSMCs remain to be fully elucidated.