| First Author | Dahiya S | Year | 2024 |
| Journal | Nat Commun | Volume | 15 |
| Issue | 1 | Pages | 3740 |
| PubMed ID | 38702347 | Mgi Jnum | J:348051 |
| Mgi Id | MGI:7639056 | Doi | 10.1038/s41467-024-47972-4 |
| Citation | Dahiya S, et al. (2024) Acinar to beta-like cell conversion through inhibition of focal adhesion kinase. Nat Commun 15(1):3740 |
| abstractText | 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. |
