作者: Paul R. Kemp , James C. Metcalfe
DOI: 10.1007/978-94-015-9321-2_20
关键词:
摘要: Smooth muscle cells play a major role in the formation of vascular lesions found atherosclerosis and restenosis injury after angioplasty [1,2]. The smooth such show reduced levels many markers differentiated state (e.g. SM22α, muscle-myosin heavy chain {SM-MHC} α-actin {Smα-actin} [3,4]). In some instances muscle-specific isoforms contractile proteins SM-MHC) are replaced by their non-muscle equivalents. addition to loss expression genes, intimal (VSMCs) express genes that associated with calcium metabolism bone tissue matrix GLA protein osteopontin [5–8]). There has been significant progress towards identifying factors involved promoting or inhibiting cell proliferation these pathologic conditions. However, little is known about mechanisms regulate this type defining phenotype [9]. Given phenotypic changes seen VSMC pathological conditions, systems which control may lesion formation.