Exploring the role of calcitonin signaling in left ventricular fibrogenesis.

Cardiofibroblasts are key players in myocardial fibrosis and structural remodelling underlying common cardiac conditions, such as hypertension. We have recently discovered that the hormone calcitonin (CT), canonically secreted by the thyroid gland and involved in bone turnover, is produced in significant quantities by atrial cardiomyocytes and acts in a paracrine fashion on neighbouring cardiofibroblasts to control their proliferation, migration and collagen processing. CT exerts its effects via CT receptors and their disruption in mice promotes atrial fibrosis and arrhythmogenesis.

In this project we aim to test whether CT signalling cascade plays a role in the regulation of ventricular fibrogenesis. We will use a combination of sophisticated molecular, RNA and cellular biology techniques, high-throughput RNA sequencing approach in native human ventricular fibroblasts and genetically modified mice. The results of this proposal will help to begin to understand the role of CT-CT receptor axis in ventricular fibrogenesis that is currently unknown.