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(Circulation Research. 1997;80:295-296.)
© 1997 American Heart Association, Inc.

Articles

Microtubules and Pressure-Overload Hypertrophy

Richard A. Walsh

Correspondence to Richard A. Walsh, MD, Director of Cardiology & Cardiovascular Center, University of Cincinnati College of Medicine, PO Box 670542, Cincinnati, OH 45267-0542 E-mail WALSHRA@UCBEH.SAN.UC.EDU

Key Words: cardiomyocyte • cytoskeleton • hypertrophy

	Introduction

 
Cardiac hypertrophy is a process whereby an increase in chamber mass occurs largely by an increase in size of terminally differentiated cardiomyocytes in response to increased external and/or internal work. Hypertrophied cardiomyocytes have abnormal electrical and mechanical properties that underlie, at least in part, altered cardiovascular function in a variety of pathological states. In particular, heart failure of diverse origins is invariably accompanied by hypertrophy, and contractile failure appears to be an inevitable consequence of hypertrophic stimuli of sufficient severity and duration. Molecular and biochemical mechanisms that are responsible for functions of the hypertrophied cardiomyocyte are being intensively studied using genetically engineered mice, animal models of human disease, and clinical investigations. These approaches have identified important alterations in myofilament and calcium-cycling proteins, sarcolemmal ion pumps, channels, and receptors and in various signal transduction pathways of hypertrophied hearts.¹

In contrast to our knowledge of the importance of alterations in proteins that actively participate in myocyte contraction, relaxation, and growth, there is less information regarding the role of cytoarchitectural components of the cardiomyocyte in normal and pathological states. The cardiomyocyte cytoskeleton is composed of myofibrillar and extramyofibrillar or cytoplasmic compartments. Biophysical interactions among sarcolemmal integrin receptors and the cytoplasmic and myofibrillar cytoskeleton are largely unknown. The myofibrillar cytoskeleton includes titin (the largest protein known and the third most abundant cardiac protein), desmin, C protein, nebulin, and vinculin.² The extramyofibrillar cytoskeleton of all eukaryotic cells, including the cardiomyocyte, is composed of an intertwined network of three classes of filamentous biopolymers: actin-containing microfilaments, intermediate . . . [Full Text of this Article]

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