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Review
. 2014;20(36):5681-9.
doi: 10.2174/1381612820666140204111236.

Signaling epicenters: the role of caveolae and caveolins in volatile anesthetic induced cardiac protection

Affiliations
Review

Signaling epicenters: the role of caveolae and caveolins in volatile anesthetic induced cardiac protection

Yousuke T Horikawa et al. Curr Pharm Des. 2014.

Abstract

Caveolae are flask-like invaginations of the cell surface that have been identified as signaling epicenters. Within these microdomains, caveolins are structural proteins of caveolae, which are able to interact with numerous signaling molecules affecting temporal and spatial dimensions required in cardiac protection. This complex moiety is essential to the mechanisms involved in volatile anesthetics. In this review we will outline a general overview of caveolae and caveolins and their role in protective signaling with a focus on the effects of volatile anesthetics. These recent developments have allowed us to better understand the mechanistic effect of volatile anesthetics and their potential in cardiac protection.

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Figures

Figure 1
Figure 1. Caveolae are signaling epicenters
Caveolae are known to concentrate various signaling receptors (receptor tyrosine kinases, RTK; G-protein coupled receptors, GPCRs; caveolin scaffolding domains, CSD) as well as caveolins which can interact with many protein kinase.
Figure 2
Figure 2. Electron microscopy of caveolae
A) Untreated cardiac myocyte; B) Caveolin-3 overexpressing cardiac myocyte have an abundance of caveolae; C) Caveolin-3.knockout cardiac myocyte lack caveolae; D) Isoflurane induces caveolae formation in cardiac myocytes; scale bar 200nm
Figure 3
Figure 3. The role of caveolae and caveolins in anesthetic induced cardiac protection
Isoflurane increases caveolae formation at the cell surface Acute preconditioning requires both caveolin-1 and -3 and activates both Src kinase and PI3K/AKT/GSK pathway, whereas delayed cardiac protection increases caveolin-3 and increases GLUT 4 expression.

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