Myocardial hypertrophy is the result of sustained perturbations to the mechanical and/or neurohormonal homeostasis of cardiac cells and is driven by integrated, multiscale biophysical and biochemical processes that are currently not well defined. In this brief review, we highlight recent computational and experimental models of cardiac hypertrophy that span mechanisms from the molecular level to the tissue level. Specifically, we focus on: (i) molecular-level models of the structural dynamics of sarcomere proteins in hypertrophic hearts, (ii) cellular-level models of excitation-contraction coupling and mechanosensitive signaling in disease-state myocytes, and (iii) organ-level models of myocardial growth kinematics and predictors thereof. Finally, we discuss how spanning these scales and combining multiple experimental/computational models will provide new information about the processes governing hypertrophy and potential methods to prevent or reverse them.
Laboratory Medicine Center, Department of Genetic and Genomic Medicine, Zhejiang Provincial People's Hospital, Affiliated People's Hospital, Hangzhou Medical College, Hangzhou, Zhejiang, China.
Background: GTPBP3 catalyzes τm(s) U biosynthesis at the 34th wobble position of mitochondrial tRNAs, the hypomodification of τmU leads to mitochondrial disease. While twenty-three variants of GTPBP3 have been reported worldwide, the genetic landscape in China remains uncertain.
Methods: By using whole-exome sequencing, the candidate individuals carrying GTPBP3 variants were screened and identified.
Extensive research is needed to examine the association between cardiovascular disease (CVD) and cancer. The observational study is based on data collected from the 2005-2018 National Health and Nutrition Examination Survey (NHANES). To assess the connection between CVDs and cancer, we used a weighted multivariable logistic regression analysis with as many confounding factors as feasible included in the model.
Background: This study aims to characterize right ventricular dysfunction (RVD) in heart failure (HF) with preserved ejection fraction and understand the cumulative prognostic value of abnormal RV echocardiographic parameters in HF with preserved ejection fraction.
Methods And Results: Data from 809 patients in the PARAGON-HF (Prospective Comparison of Angiotensin Receptor-Neprilysin Inhibitor With Angiotensin-Receptor Blocker Global Outcomes in HF With Preserved Ejection Fraction) echocardiographic substudy (55% women, mean age 74±8 years) were analyzed. Correlates of RVD (defined as tricuspid annular plane systolic excursion <1.
Background: Aortic valve stenosis (AVS) is a progressive disease characterized by fibrosis, inflammation, calcification, and stiffening of the aortic valve leaflets, leading to disrupted blood flow. If untreated, AVS can progress to heart failure and death within 2 to 5 years. Uncovering the molecular mechanisms behind AVS is key for developing effective noninvasive therapies.
Background: This study compared the risks of atherothrombotic major adverse cardiovascular events in patients with type 2 diabetes taking SGLT2 (sodium-glucose cotransporter 2) inhibitors to those taking DPP-4 (dipeptidyl peptidase-4) inhibitors.
Methods And Results: All adult patients (≥18 years of age) with type 2 diabetes and newly prescribed with SGLT2 inhibitors or DPP-4 inhibitors across all public hospitals in Hong Kong between January 2015 and December 2019 were included. Patients were propensity matched in a 1:1 ratio using a caliper distance of 0.
