Burns C. Blaxall

TL;DR: Current knowledge regarding the origins and roles of fibroblasts, mediators and signaling pathways known to influence fibroblast function after myocardial injury are summarized, as well as novel therapeutic strategies under investigation to attenuate cardiac fibrosis are summarized.

TL;DR: These same lineage-traced initial fibroblasts persisted within the scar, achieving a new molecular and stable differentiated state referred to as a matrifibrocyte, which was also observed in the scars of human hearts.

TL;DR: Cardiac-directed overexpression of the human beta(1)-AR in transgenic mice leads to a significant histopathological phenotype with no apparent functional consequence in younger mice and a variable degree of cardiac dysfunction in older animals, which may ultimately prove useful for investigating the biological basis of adrenergically-mediated myocardial damage in humans.

TL;DR: The research priorities outlined in this document are meant to stimulate scientific advances in HFpEF by providing a road map for future collaborative investigations among a diverse group of scientists across multiple domains.

TL;DR: It is suggested that PDE3A reduction and consequent inducible cAMP early repressor induction are critical events in Ang II– and isoproterenol-induced cardiomyocyte apoptosis and may contribute to the development of heart failure.