Abstract
Gap junctions are intercellular channels made of connexin proteins, mediating both electrical and biochemical signals between cells. The ability of gap junction proteins to regulate immune responses, cell proliferation, migration, apoptosis and carcinogenesis makes them attractive therapeutic targets for treating inflammatory and neoplastic disorders in different organ systems. Alterations in gap junction profile and expression levels are observed in hyperproliferative skin disorders, lymphatic vessel diseases, inflammatory lung diseases, liver injury and neoplastic disorders. It is now recognized that the therapeutic effects mediated by traditional pharmacological agents are dependent upon gap junction communication and may even act by influencing gap junction expression or function. Novel strategies for modulating the function or expression of connexins, such as the use of synthetic mimetic peptides and siRNA technology are considered.
Highlights
WONG et al: THE ROLE OF GAP JUNCTIONS IN INFLAMMATORY AND NEOPLASTIC DISORDERS states, and the use of gap junction modulators in different clinical conditions [24]
Apart from modifying gap junction function, interventions can be applied through modulating synthesis, transport, assembly, phosphorylation, and degradation of gap junction proteins [25]
This review focuses on reviewing the therapeutic applications of gap junction modulators in inflammatory and neoplastic disorders
Summary
Several autosomal dominant hereditary epidermal diseases are attributed to mutations in genes encoding for connexins. These diseases include Vohwinkel syndrome, Bart‐Pumphrey syndrome, hystrix‐like ichthyosis with deafness syndrome, keratitis‐ichthyosis‐deafness (KID) syndrome, erythrokeratoderma variabilis, hidrotic ectodermal dysplasia and oculodentodigital dysplasia [27,28]. 10 missense substitution mutations in the Cx26 gene are known to cause KID syndrome [32]. Retinoic acid is a prospect for novel treatment in hyperkeratotic skin. It unexpectedly causes: i) significant Cx26 upregulation; ii) Cx43 upregulation; and iii) increased epidermal thickness [34]. The mechanisms by which elevated Cx26 expression results in beneficial therapeutic effects in KID syndrome without exacerbating this condition remain unknown. The precise underlying mechanism of action will need to be understood before further testing
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