In Person Special Seminar: Involvement of Non-canonical Inflammatory Response in Tissue Dysfunction of Several Chronic Diseases
David Crossman, Ph.D.
Academic Director, Biomedical Research Imaging Unit
Senior Research Fellow, Heart Foundation of New Zealand
Cardiac Nanobiology Research Group
Department of Physiology
School of Medical Sciences
Waipapa Taumata Rau | The University of Auckland
In Person Seminar: Fibrosis and Aberrant Ca2+ Handling in the Failing Heart
Date: Feb. 15, 2024
Time: 11 a.m.
About this Seminar
Fibrosis and aberrant Ca2+ handling are hallmarks of heart failure but are considered separate features. However, the fibrotic disposition of nanometer-sized collagen fibrils, particularly collagen VI (ColVI), may directly diminish Ca2+signalling in human heart failure. Using super-resolution microscopy Dr. Crossman and his team found increased ColVI within the transverse(t)-tubules. Moreover, t-tubule remodeling disrupts Ca2+ signaling in heart failure. Recently, circulating levels of ColVI were found to independently associate with poor outcomes in heart failure. While the importance of ColVI to skeletal muscle function is underscored by its mutation causing muscular dystrophy, its role in cardiac contraction remains poorly understood. Significantly, muscular dystrophy patients often develop heart failure. To understand the role of ColVI in the heart the lab created a knockout of this gene in the rat (Col6a1-/-). Echocardiography showed both impaired systolic and diastolic function. Cardiac myocytes from Col6a1-/- have increased systolic Ca2+transient and greater response to b-adrenergic stimulation that is pro-arrhythmogenic. Similar disturbance in Ca2+ handling is found in the cardiac myocytes of the mdx mouse which has non-functional dystrophin supporting our hypothesis that ColVI is part of the dystrophin-glycoprotein-complex and may have a role in regulating Ca2+ dynamics.
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