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DYRK1A kinase inhibitors promote β-cell survival and insulin homeostasis

Permanent lenke
https://hdl.handle.net/10037/23632
DOI
https://doi.org/10.3390/cells10092263
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Åpne
article.pdf (10.12Mb)
Publisert versjon (PDF)
Dato
2021-08-31
Type
Journal article
Tidsskriftartikkel
Peer reviewed

Forfatter
Barzowska, Agata; Pucelik, Barbara; Pustelny, Katarzyna; Matsuda, Alex; Martyniak, Alicja; Stępniewski, Jacek; Maksymiuk, Anna; Dawidowski, Maciej; Rothweiler, Ulli; Dulak, Józef; Dubin, Grzegorz; Czarna, Anna
Sammendrag
The rising prevalence of diabetes is threatening global health. It is known not only for the occurrence of severe complications but also for the SARS-Cov-2 pandemic, which shows that it exacerbates susceptibility to infections. Current therapies focus on artificially maintaining insulin homeostasis, and a durable cure has not yet been achieved. We demonstrate that our set of small molecule inhibitors of DYRK1A kinase potently promotes β-cell proliferation, enhances long-term insulin secretion, and balances glucagon level in the organoid model of the human islets. Comparable activity is seen in INS-1E and MIN6 cells, in isolated mice islets, and human iPSCderived β-cells. Our compounds exert a significantly more pronounced effect compared to harmine, the best-documented molecule enhancing β-cell proliferation. Using a body-like environment of the organoid, we provide a proof-of-concept that small–molecule–induced human β-cell proliferation via DYRK1A inhibition is achievable, which lends a considerable promise for regenerative medicine in T1DM and T2DM treatment.
Forlag
MDPI
Sitering
Barzowska, Pucelik, Pustelny, Matsuda, Martyniak, Stępniewski, Maksymiuk, Dawidowski, Rothweiler, Dulak, Dubin, Czarna. DYRK1A kinase inhibitors promote β-cell survival and insulin homeostasis. Cells. 2021;10(9)
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  • Artikler, rapporter og annet (UB) [3244]
Copyright 2021 The Author(s)

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