{'fraction_non_alphanumeric': 0.02775290957923008, 'fraction_numerical': 0.0026857654431512983, 'mean_word_length': 5.245810055865922, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Bone marrow-derived smooth muscle cells are breaking bad in atherogenesis.

Vascular smooth muscle cells (SMCs) are highly specialized in contraction, thus regulating the vascular tone. In contrast to other muscle cells, however, SMCs can reversibly undergo quite drastic phenotypic changes in response to environmental signals.1 Following vascular injury, for instance, the expression of contractile proteins in SMCs substantially declines and these cells adopt a “synthetic” phenotype.2 The origin of cells expressing SMC-specific markers in neointimal lesions or atherosclerotic plaques is known to be heterogeneous. The long-standing paradigm that these SMC-like cells migrate from the media into the intima on injury has been challenged on the grounds that it may not be the only explanation of their provenience. Namely, seminal work by Sata et al3 has provided evidence that—at least partly and depending on the degree of injury—SMC-like cells in different forms of arterial plaque development are derived from the bone marrow (BM). The extent to which BM-derived SMCs (BM-SMCs) contribute to the cellularity …