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Dahiya, S.* ; Saleh, M.* ; Rodriguez, U.A.* ; Rajasundaram, D.* ; R. Arbujas, J.* ; Hajihassani, A.* ; Yang, K. ; Sehrawat, A.* ; Kalsi, R.* ; Yoshida, S.* ; Prasadan, K.* ; Lickert, H. ; Hu, J.* ; Piganelli, J.D.* ; Gittes, G.K.* ; Esni, F.*

Acinar to β-like cell conversion through inhibition of focal adhesion kinase.

Nat. Commun. 15:3740 (2024)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Insufficient functional beta-cell mass causes diabetes; however, an effective cell replacement therapy for curing diabetes is currently not available. Reprogramming of acinar cells toward functional insulin-producing cells would offer an abundant and autologous source of insulin-producing cells. Our lineage tracing studies along with transcriptomic characterization demonstrate that treatment of adult mice with a small molecule that specifically inhibits kinase activity of focal adhesion kinase results in trans-differentiation of a subset of peri-islet acinar cells into insulin producing beta-like cells. The acinar-derived insulin-producing cells infiltrate the pre-existing endocrine islets, partially restore beta-cell mass, and significantly improve glucose homeostasis in diabetic mice. These findings provide evidence that inhibition of the kinase activity of focal adhesion kinase can convert acinar cells into insulin-producing cells and could offer a promising strategy for treating diabetes. A cure for diabetes could entail an effective cell replacement therapy through generation of new insulinproducing cells. In this study, we show that inhibition of focal adhesion kinase activity results in transdifferentiation of a subset of peri-islet acinar cells into functional insulin producing beta-like cells.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Pancreatic Exocrine Cells; Alpha-cells; Proliferation; Regeneration; Islets; Fak; Endocrine; Insulin; Dark; Mice
Sprache englisch
Veröffentlichungsjahr 2024
HGF-Berichtsjahr 2024
ISSN (print) / ISBN 2041-1723
e-ISSN 2041-1723
Zeitschrift Nature Communications
Quellenangaben Band: 15, Heft: 1, Seiten: , Artikelnummer: 3740 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Regeneration Research (IDR)
POF Topic(s) 90000 - German Center for Diabetes Research
30201 - Metabolic Health
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-501900-231
G-502300-001
Förderungen Cochrane-Weber Endowed Funds for Diabetes Research
Research Advisory Committee (RAC) Children's Hospital of Pittsburgh of UPMC
JDRF
Children's Hospital
U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID)
DOI 10.1038/s41467-024-47972-4
WOS ID 001214215100004
WOS ID 001214215100003
PubMed ID 38702347
Erfassungsdatum 2024-06-05
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