Arteriosclerosis, Thrombosis, and Vascular Biology. 1997;17:417-422
© 1997 American Heart Association, Inc.
Articles |
Vascular Myofibroblasts
Lessons From Coronary Repair and Remodeling
From the Department of Medicine (Cardiology), Thomas Jefferson University, Philadelphia, Pa.
Correspondence to Andrew Zalewski, MD, Cardiovascular Research Center, Division of Cardiology, Thomas Jefferson University, 1025 Walnut St, Suite 410N, Philadelphia, PA 19107.
Key Words: coronary artery • myofibroblast • smooth muscle • adventitia
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Introduction |
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Vascular repair and remodeling represents a common theme of many cardiovascular abnormalities. This is not surprising, since frequent exposure of blood vessels to excessive hemodynamic stress (eg, hypertension), the noxious effects of blood contents (eg, atherogenic lipids), and locally released cytokines (eg, postangioplasty) require readily available mechanism(s) to counteract their adverse effects and to preserve the intactness of the vessel wall. These responses, which were evolutionarily developed to repair an injured tissue, often escape self-limiting control and result in lumen narrowing. Various vascular lesions contain mesenchymal cells, different from normal medial cells, which has been viewed as evidence that smooth muscle (SM) cells modulate their phenotype in response to changes in the environment in situ.1 2 3 This concept has been further reinforced by the dedifferentiation of SM cells to a "synthetic" phenotype in culture.4 The presence of "nonmuscle" cells in the normal vessel wall, however, raises an intriguing question regarding whether they contribute to vascular repair while acquiring markers of muscle differentiation. This review will examine the potential role of these cells in coronary repair and remodeling.
Seminal studies by Gabbiani and coworkers5 6 have
established that wound healing is associated with rapid activation of
fibroblasts, which proliferate, migrate, and undergo differentiation to
myofibroblasts. These cells acquire bundles of microfilaments (stress
fibers) and develop extensive connections with the surrounding
extracellular matrix, a change which is consistent with the primary
role of newly formed myofibroblasts to close an open wound by means of
extracellular matrix protein synthesis and contraction.7
Subsequent studies have confirmed
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