Are fibrous and lipid-rich atherosclerotic plaques part of interchangeable morphologies related to inflammation : a concept?
Our observations support the concept that inflammatory mechanisms modulate plaque morphology, by promoting either synthesis or lysis of the fibrous cap. Our hypothesis is that fibrous and atheromatous lesions are essentially interchangeable.
These finding strongly suggest that PTHLH represses the induction of human decidualization, stimulates stromal cell apoptosis, and limits the extent of uterine stromal cell differentiation. Because PTHLH and its receptor are expressed by HUF cells and placental cells, the inhibitory effect of PTHLH on decidualization appears to be due, at least in part, to an autocrine/paracrine mechanism.