Abstract
The growing interest in smooth muscle cell (SMC) biology originates in morphological studies demonstrating that SMCs are prominent constituents of the “proliferative early lesion” of atherosclerosis. This disease still accounts for more than 50% of all deaths in highly industrialized countries [22, 23, 27, 36, 37]. In addition, abnormal SMC proliferation has been observed in several other clinically important diseases such as subacute and chronic forms of arthritis and in graft versus host disease in transplanted kidneys [30; reviewed by 9]. While the proliferation of SMCs during embryonal angiogenesis is confined to the media of the arterial wall [32], the irregular growth of SMCs in atherosclerosis is characterized by the presence of multiple layers of proliferating SMCs in the intima [23, 27]. The mechanisms underlying the accumulation of SMCs in the intima are not yet known but are assumed to be the result of the interaction between the SMCs, monocytes/macrophages, lymphocytes, and endothelial cells [23, 27]. These morphological characteristics of the early lesions of atherosclerosis resemble in many respects a chronic inflammatory reaction [8, 30].
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Janßen-Timmen, U., Salbach, P., Gronwald, R., Habenicht, A.J.R. (1990). Growth Factors for Smooth Muscle Cells. In: Piper, H.M. (eds) Cell Culture Techniques in Heart and Vessel Research. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-75262-9_23
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DOI: https://doi.org/10.1007/978-3-642-75262-9_23
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