Intimal hyperplasia is the thickening of the tunica intima of a blood vessel as a complication of a reconstruction procedure or endarterectomy.[1] Intimal hyperplasia is the universal response of a vessel to injury. It is a restenosis and this is an important reason of late bypass graft failure, particularly in vein and synthetic vascular grafts.[2]
Cause
editIntimal hyperplasia is due to a dysfunction of endothelial cells which results in a reprogramming of the vascular smooth muscle cells (VSMCs). As a result, VSMCs proliferate and change their phenotype.[3]
Possible treatment
editA possible treatment to avoid this could be hydrogen sulfide. Hydrogen sulfide (H2S) works as a vasculoprotective gasotransmitter in the human body but is also tested to reduced intimal hyperplasia. There are different kinds of H2S donors: NaHS (the reference in scientific literature despite the fact it is too toxic to use it in human patients) and STS (already used in patient to treat cyanide poisoning).
See also
editReferences
edit- ^ Kaban, Leonard B. (1 January 2004). "CHAPTER 20 - Acquired Abnormalities of the Temporomandibular Joint". Pediatric Oral and Maxillofacial Surgery. W.B. Saunders. pp. 340–376. ISBN 978-0-7216-9691-1. Retrieved 20 October 2021.
- ^ Haruguchi, Hiroaki; Teraoka, Satoshi (2003). "Intimal hyperplasia and hemodynamic factors in arterial bypass and arteriovenous grafts: a review". Journal of Artificial Organs. 6 (4): 227–235. doi:10.1007/s10047-003-0232-x. ISSN 1434-7229. PMID 14691664. S2CID 24921182.
- ^ Déglise, Sébastien; Bechelli, Clémence; Allagnat, Florent (2022). "Vascular smooth muscle cells in intimal hyperplasia, an update". Frontiers in Physiology. 13: 1081881. doi:10.3389/fphys.2022.1081881. ISSN 1664-042X. PMC 9845604. PMID 36685215.
External links
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