Targeting STAT3 provides a potential therapeutic strategy for obstructive sleep apnea-related fibrotic heart disease mediated by TSP1.

In models reconstructed from MRI scans of patients with embolic stroke of undetermined source, computational simulations reveal that fibrosis has the intrinsic capacity to sustain arrhythmia drivers when subjected to triggered activity known to exist in patients with atrial fibrillation.

Comprehensive scRNA-seq analysis of cardiac stromal cells in healthy and injured hearts reveals novel cell types and non-linear cell dynamics, providing new insights into cardiac inflammation, fibrosis and repair.

Lymphangiogenic therapy VEGFCc156s improved angiotensin-II-induced impairments in heart function via novel mechanisms, which include transcriptional responses to alleviate inflammation and cardiac fibrosis, and systemic responses to ameliorate hypertension.

Human cardiac fibroblasts regulate their cellular responses according to the combination of multiple environmental stimuli namely oxygen changes and mechanical signals.

Mechanotransduction signaling analysis suggests that mechanical tension can sensitize, desensitize, and reverse cell responses to biochemical agonists, as well as provide mechano-adaptive targets for regionally specific drug responses.

Cardiac intercellular communication plays a critical role in diabetic myocardial fibrosis and specific targeting of Hrc^hi fibroblasts may be a potential therapeutic target for diabetic cardiomyopathy.

Cardiac fibroblast reduction is well-tolerated and demonstrates beneficial outcomes after heart injury.

A novel computational approach integrates personal genetics into personalized whole heart digital twins to predict ventricular arrhythmia circuits for patients with arrhythmogenic right ventricular cardiomyopathy.

Vigorous endurance training results in prolongation of cardiac repolarization and increased repolarization instability, mild ventricular fibrosis associated with decrease of the transient outward potassium current, and enhanced arrhythmia susceptibility in canine model.