Activation, Proliferation and Migration of Endothelial Cells under Normal and Pathological Conditions
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".
Deadline for manuscript submissions: 26 July 2024 | Viewed by 231
Special Issue Editor
Interests: intracellular transport Golgi complex; endothelium, atherosclerosis; electron microscopy
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Vascular endothelium is found in almost all organs and tissues. Its role in understanding the mechanisms of various diseases is difficult to overestimate. This became especially clear after the COVID-19 epidemic, when, due to the similarity of the protein composition of the receptors of the ciliated cells of the airways and vascular endothelium, various, and often very severe, complications developed following the disease. It has long been known that the endothelium of elastic-type arteries is involved in the pathogenesis of atherosclerosis, and the endothelium of this and other parts of the vascular bed is involved in the pathogenesis of many other diseases. Knowledge of the mechanisms associated with damage to this endothelium and its subsequent repair is very important now. Although tremendous progress has been made recently in deciphering the molecular mechanisms of vascular endothelium functioning. Most of these discoveries were made in vitro. It is necessary to bring this knowledge to the tissue level. Additionally, rather little information is available on the role of itracell, ulat transport and endocytosis within endothelial cells. We would greatly appreciate all researchers who take the time to contribute to this Special Issue.
Prof. Dr. Alexandre Mironov
Guest Editor
Manuscript Submission Information
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Keywords
- endothelial cell
- regeneration
- angiogenesis
- migration
- molecular mechanism
- intracellular transport
- Golgi
- signaling
- transcription
- miRNA
- tumorigenesis
- COVID
