Eva A. Rog-Zielinska

TL;DR: The results reveal a molecular mechanism by which lipid overload-induced mitochondrial ROS generation causes mitochondrial dysfunction by inducing post-translational modifications of mitochondrial proteins that regulate mitochondrial dynamics.

TL;DR: Direct electrophysiological evidence of heterocellular electrotonic coupling in native myocardium is provided and tunneling nanotubes are identified as a possible substrate for electrical cell coupling that may be in addition to previously discovered connexins at sites of myocyte–nonmyocyte contact in the heart.

TL;DR: It is shown that activation of the peroxisome proliferator–activated receptor γ (PPARγ) via pioglitazone treatment protects against heart failure in the Sugen hypoxia rat model of pulmonary arterial hypertension and suggests that targeting PPARγ activation to restore fatty acid oxidation could be therapeutic for pulmonary hypertension and other diseases with altered lipid metabolism.

TL;DR: It is demonstrated that structural, functional and biochemical maturation of the foetal heart is dependent on glucocorticoid signalling within cardiomyocytes and vascular smooth muscle, though some aspects of heart maturation are independent of GR at these key sites.

TL;DR: A better understanding of fibroblasts' biophysical interactions will help to target scar structure and function, and will facilitate the development of novel therapies aimed at modifying scar properties for patient benefit.