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The Cardiovascular Continuum describes a sequence of events from cardiovascular risk factors to end‐stage heart disease. It includes conventional pathologies affecting cardiovascular functions such as hypertension, atherosclerosis or thrombosis and was traditionally considered from the metabolic point of view. This Cardiovascular Continuum, originally described by Dzau and Braunwald, was extended by O'Rourke to consider also the crucial role played by degradation of elastic fibers, occurring during aging, in the appearance of vascular stiffness, another deleterious risk factor of the continuum. However, the involvement of the elastin degradation products, named elastin‐derived peptides, to the Cardiovascular Continuum progression has not been considered before. Data from our laboratory and others clearly showed that these bioactive peptides are central regulators of this continuum, thereby amplifying appearance and evolution of cardiovascular risk factors such as diabetes or hypertension, of vascular alterations such as atherothrombosis and calcification, but also nonalcoholic fatty liver disease and nonalcoholic steatohepatitis. The Elastin Receptor Complex has been shown to be a crucial actor in these processes. We propose here the participation of these elastin‐derived peptides and of the Elastin Receptor Complex in these events, and introduce a revisited Cardiovascular Continuum based on their involvement, for which elastin‐based pharmacological strategies could have a strong impact in the future. [ABSTRACT FROM AUTHOR]

Regulation of annexing concentration and localization were investigated in thyroid tissues of hypothyroid [methylthiouracil (MeSur) treatment], euthyroid (control) and hyperthyroid [thyroxine (T4) treatment] rats. A low level of circulating thyroid hormones induces a decrease of total thyroid calcium-binding protein concentration when compared with the concentration in unstimulated animals. Conversely, concentrations of annexing I, II and V increase. The accumulation of these proteins in two subcellular compartments (cytosolic and particulate fractions) can be reversed by addition of thyroid hormones. The finding of a specific increase in annexing concentration in thyroid-hormone-deficient rats, with a general decrease of the total calcium-binding protein content points to a very important role of these proteins in the cells Furthermore, hyperthyroidism gives opposite results. To investigate the transduction pathway of annexing I-, II- and V-induced biosynthesis by thyroid hormones in thyroid glands, we used cultured pig thyroid cells as in vitro model system. In previous work, we have shower that annexing concentrations and localization are under TSH control via the adenylate cyclase pathway. In the presence of MeSur (in the culture medium), the protein-binding iodine remains low, indicative of weak thyroid hormone synthesis (data not shown) and that the annexing content is unchanged. These results suggest that, in thyroid tissue, an indirect mechanism links thyroid hormones to annexing expressions via the TSH feed-back loop, and excludes autocrine regulation. [ABSTRACT FROM AUTHOR]