PMC:7565665 / 68143-69313 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7565665","sourcedb":"PMC","sourceid":"7565665","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7565665","text":"Studies exploring cysteamine-dendrimers have revealed similar results. Two of our recent studies demonstrated that cysteamine-based dendrimers were able to not only decrease ΔF508-CFTR aggregation, but also rescue the protein to increase the plasma membrane expression [45,149]. Moreover, these investigations showed that this recue of CFTR by the cysteamine-dendrimers alleviated the autophagy impairment associated with the ΔF508-CFTR mutation [45,149]. This alleviation of CFTR-autophagy impairment was further shown to increase the clearance and killing of P. aeruginosa in both studies [45,149]. Hence, cysteamine-based dendrimers provide a therapeutic option in the treatment of both acute and chronic exacerbations in CF. Cysteamine’s dendrimer-based formulation also proved beneficial for clearing P. aeruginosa, and thus has potential for treating other infections in CF and non-CF patients who are prone to exacerbations. The added advantage of this intervention strategy is that exacerbations in respiratory diseases including those with CFTR dysfunction may be treated and prevented without antibiotics, where multidrug-resistant (MDR) infections are 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