ArticleCell death & disease2026
RIP kinase inhibition with Necrostatin-1 improves human marginal mass islet graft survival and function for the management of type 1 diabetes.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Islet transplantation (ITx) has demonstrated that cellular therapies can improve glycemic control in patients with type 1 diabetes. However, cell death in the acute post-transplant period accounts for the loss of up to 70% of the islets, resulting in the requirement of multiple donors per recipient to achieve normoglycemia. Several studies have targeted apoptosis prevention after ITx; herein, our study explores a novel approach by modulating RIPK1-associated stress pathways using Necrostatin-1 (Nec-1) to enhance human islet survival, engraftment, and function post-transplant. Nec-1 treatment for 24 h prior to transplant significantly reduced the expression of RIPK1 (p = 0.0021) and RIPK3 (p = 0.0042), resulting in decreased cell death (p < 0.0001) and necroptosis (p < 0.0001), measured as TUNEL
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