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.
No takes yet. Share an insight, caveat, or question.
Kalinina et al. (2004) studied this question.
Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context: