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- W3037868802 abstract "Thiopeptide antibiotics are emerging clinical candidates that exhibit potent antibacterial activity against a variety of intracellular pathogens, including Mycobacterium tuberculosis (Mtb). Many thiopeptides directly inhibit bacterial growth by disrupting protein synthesis. However, recent work has shown that one thiopeptide, thiostrepton (TSR), can also induce autophagy in infected macrophages, which has the potential to be exploited for host-directed therapies against intracellular pathogens, such as Mtb. To better define the therapeutic potential of this class of antibiotics, we studied the host-directed effects of a suite of natural thiopeptides that spans five structurally diverse thiopeptide classes, as well as several analogs. We discovered that thiopeptides as a class induce selective autophagic removal of mitochondria, known as mitophagy. This activity is independent of other biological activities, such as proteasome inhibition or antibiotic activity. We also find that many thiopeptides exhibit potent activity against intracellular Mtb in macrophage infection models. However, the thiopeptide-induced mitophagy occurs outside of pathogen-containing autophagosomes and does not appear to contribute to thiopeptide control of intracellular Mtb. These results expand basic understanding of thiopeptide biology and provide key guidance for the development of new thiopeptide antibiotics and host-directed therapeutics." @default.
- W3037868802 created "2020-07-02" @default.
- W3037868802 creator A5008419334 @default.
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- W3037868802 creator A5056713989 @default.
- W3037868802 creator A5070615711 @default.
- W3037868802 creator A5081419672 @default.
- W3037868802 date "2020-06-26" @default.
- W3037868802 modified "2023-09-26" @default.
- W3037868802 title "Thiopeptides Induce Proteasome-Independent Activation of Cellular Mitophagy" @default.
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- W3037868802 doi "https://doi.org/10.1021/acschembio.0c00364" @default.
- W3037868802 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7442609" @default.
- W3037868802 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32589399" @default.
- W3037868802 hasPublicationYear "2020" @default.