The impact of progesterone on the cardiovascular system is relevant, but not as well characterized as the effects of estrogens. The recent early interruption of the conjugated equine estrogens (CEE)-medroxyprogesterone acetate (MPA) arm of the Women's Health Initiative trial, but not of the parallel CEE-only treatment arm, suggesting the possibility of harmful cardiovascular effects of the progestins, boosts the debate on the role of progesterone and progestins on the vascular tree. The data available up to now show the presence of important regulatory effects of progestagens on vascular cells. Additionally, the presence of a progestagen results in diverse modifications of the effects of estrogens, sometimes acting synergically, others being neutral or antagonizing estrogens' effects. Notwithstanding the availability of consistent observations on the functional effects of progestins on the cardiovascular system, the molecular mechanisms of progestins actions on vascular cells have been up to now only scarcely characterized. Novel mechanisms of signal transduction are being discovered for progesterone receptors in different tissues, some of which are independent of gene transcription regulation, and are therefore indicated as "nongenomic." Furthermore, the contribution to signal transduction of co-activators is currently widely investigated, in order to understand the ways to tissue-specificity and to engineer new progesterone receptor modulators. The understanding of the molecular basis of progesterone receptor signaling in vascular tissue is therefore of paramount importance for the development of hormonal agents with an optimal cardiovascular profile.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.steroids.2003.08.006 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Annual epidemics of influenza result in 3-5 million cases of severe illness and more than 600 000 deaths. Severe forms of influenza are usually characterized by vascular endothelial cells damage. Thus, influenza A viruses, including subtypes A(H1N1)pdm09, A(H3N2), as well as highly pathogenic avian influenza viruses, can infect the vascular endothelium, leading to activation and subsequent dysfunction of these cells.
View Article and Find Full Text PDFPeptide Nanofibers and Skin Regeneration.
Adv Exp Med Biol
January 2025
Requalite GmbH, Gräfelfing, Germany.
Peptide nanofibers have been attractive targets for regenerative medicine applications due to their tailorability to be easily functionalized for specific bioactivity, biocompatibility, ease of synthesis, adjustability of their physicochemical characteristics, and lack of biological contamination. Research groups have investigated their use for the regeneration of various tissues, such as bone, cartilage, brain, peripheral nerves, cardiac tissue, vascular tissues, endocrine cells, muscles, etc., for the treatment of degenerative diseases or tissue loss due to accidents or aging.
View Article and Find Full Text PDFTraumatic brain injury causes early aggregation of beta-amyloid peptides and NOTCH3 reduction in vascular smooth muscle cells of leptomeningeal arteries.
Acta Neuropathol
January 2025
Department of Clinical Sciences, Lund Brain Injury Laboratory for Neurosurgical Research, Lund University, 222 20, Lund, Sweden.
Traumatic brain injury (TBI) often leads to impaired regulation of cerebral blood flow, which may be caused by pathological changes of the vascular smooth muscle cells (VSMCs) in the arterial wall. Moreover, these cerebrovascular changes may contribute to the development of various neurodegenerative disorders such as Alzheimer's-like pathologies that include amyloid beta aggregation. Despite its importance, the pathophysiological mechanisms responsible for VSMC dysfunction after TBI have rarely been evaluated.
View Article and Find Full Text PDFWhile key for pathogen immobilization, neutrophil extracellular traps (NETs) often cause severe bystander cell/tissue damage. This was hypothesized to depend on their prolonged presence in the vasculature, leading to cytotoxicity. Imaging of NETs (histones, neutrophil elastase, extracellular DNA) with intravital microscopy in blood vessels of mouse livers in a pathogen-replicative-free environment (endotoxemia) led to detection of NET proteins attached to the endothelium for months despite the early disappearance of extracellular DNA.
View Article and Find Full Text PDFImplications of Raftlin in different diseases: from molecular biology to diagnostic value.
Biomark Med
January 2025
Department of Clinical Laboratory, Gansu Provincial Clinical Research Center for Laboratory Medicine, Lanzhou, China.
Raftlin (raft-linking) protein is an essential component of the lipid raft structure and plays a crucial role in B and T cell signaling pathways. It facilitates B cell receptor (BCR) signaling by promoting calcium mobilization and tyrosine phosphorylation in the cells while colocalizing with BCR on the cell membrane. Interestingly, Raftlin is internalized in lipopolysaccharide-stimulated T cells by colocalization with Toll-like receptor 4 (TLR4), wherein it exerts a similar role as in B cells.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!