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In human atherosclerotic lesions, the actions of TGF-beta appear restricted to SMCs in fibrous plaques and macrophages in fatty streaks/fibrofatty lesions. The lack of key TGF-beta signaling components in SMCs of fibrofatty lesions indicates impaired ability of these cells to initiate TGF-beta-mediated Smad-dependent transcriptional responses.
Kalinina et al. (Tue,) studied this question.
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