Abstract
Muscle cells could be briefly divided into skeletal muscular cells and smooth muscle cells in definition. While skeletal muscles were described in the previous chapter, so this article pays attention to the dedifferentiation issue of smooth muscle cell. Vascular smooth muscle cells (SMCs) retain remarkable plasticity to alternate from a differentiated to a dedifferentiated phenotype at local environmental cues or distinct developmental phases. The cellular switching process of SMCs from a quiescent contractile differentiated phenotype connected with smooth muscle-specific marker genes’ high expression, like smooth muscle 22α, calponin and α-smooth muscle actin, to a synthetic dedifferentiated phenotype associated with the marker genes’ diminished levels plays a decisive part in a large number of proliferative vascular diseases. This phenotypic alteration is regarded as essential for vascular repair. For assorted cardiovascular diseases, the inhibition of abnormal switching and the control of SMC proliferation, nonetheless, are crucial therapeutic strategies. Smooth muscle cells have demonstrated as one ideal research model for phenotypic modulation, dedifferentiation, redifferentiation, cellular plasticity, and switching. Owing to the high incidence and mortality of atherosclerosis, various researchers have devoted themselves into smooth muscle cell-related researches. This review has summed up the current knowledges of blood vessel repair, smooth muscle cell differentiation, and dedifferentiation. Transcription factors, epigenetic modulations, and miRNAs are illustrated as underlying molecular mechanisms.
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Fu, X., Zhao, A., Hu, T. (2018). Blood Vessel Repair, Atherosclerosis, and Dedifferentiation. In: Cellular Dedifferentiation and Regenerative Medicine. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-56179-9_8
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DOI: https://doi.org/10.1007/978-3-662-56179-9_8
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