About the Experimental Cardiology laboratory
Along the course of heart disease, myocardial fibrosis and inflammation present irrespective of aetiology forming a major part of cardiac remodeling with adverse functional consequences. While contributing to diastolic and systolic dysfunction, cardiac fibrosis is regarded as a pivotal arrhythmic substrate. There is also strong evidence for a role of inflammatory signalling in promoting fibrogenesis and arrhythmias.
Research conducted in this laboratory is to address some fundamental questions on the pathophysiology of cardiac fibrosis and inflammation with the aim of providing insights into clinical characterisation of cardiac fibrosis and inflammation for risk stratification and corresponding therapies. We have been particularly interested in identifying factors that contribute to cardiac inflammation and fibrogenesis with consequent adverse remodelling in settings of cardiomyopathy and ischemic heart disease.
Methodologies used include:
- Microsurgery for induction of heart diseases in mice.
- Echocardiography (non-invasive functional assessment).
- Micromanometry (hemodynamics).
- Radiotelemetry for assessment of conscious in vivo cardiovascular parameters.
- Immunohistochemistry and quantitative histology.
- Flow cytometry.
- Routine cellular and biochemical assays.
Significant recent findings and current research focus include:
- Demonstration that post-infarct cardiac inflammation is responsible for development of acute ventricular remodelling and wall rupture.
- Identification of pivotal role of platelets and macrophage migration inhibitory factor (MIF) in initiating post-infarct inflammatory responses.
- Demonstration of a robust upregulation of galectin-3 in cardiomyopathic models and galectin-3 upregulation by β-adrenergic activation.
- First documentation of microvascular leakage (or hyper-permeability) is one of the major types of myocardial injury following ischemia-reperfusion.
- Identification of MIF as a new cardiac biomarker.