
Measuring passive myocardial stiffness in D rosophila melanogaster to investigate diastolic dysfunction
Author(s) -
Kaushik Gaurav,
Zambon Alexander C.,
Fuhrmann Alexander,
Bernstein Sanford I.,
Bodmer Rolf,
Engler Adam J.,
Cammarato Anthony
Publication year - 2012
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/j.1582-4934.2011.01517.x
Subject(s) - drosophila melanogaster , diastole , myocyte , cardiology , drosophila (subgenus) , medicine , sarcomere , biology , stiffness , arterial stiffness , microbiology and biotechnology , genetics , materials science , gene , blood pressure , composite material
Aging is marked by a decline in LV diastolic function, which encompasses abnormalities in diastolic relaxation, chamber filling and/or passive myocardial stiffness. Genetic tractability and short life span make D rosophila melanogaster an ideal organism to study the effects of aging on heart function, including senescent‐associated changes in gene expression and in passive myocardial stiffness. However, use of the D rosophila heart tube to probe deterioration of diastolic performance is subject to at least two challenges: the extent of genetic homology to mammals and the ability to resolve mechanical properties of the bilayered fly heart, which consists of a ventral muscle layer that covers the contractile cardiomyocytes. Here, we argue for widespread use of D rosophila as a novel myocardial aging model by (1) describing diastolic dysfunction in flies, (2) discussing how critical pathways involved in dysfunction are conserved across species and (3) demonstrating the advantage of an atomic force microscopy‐based analysis method to measure stiffness of the multilayered D rosophila heart tube versus isolated myocytes from other model systems. By using powerful D rosophila genetic tools, we aim to efficiently alter changes observed in factors that contribute to diastolic dysfunction to understand how one might improve diastolic performance at advanced ages in humans.