ArticleDiabetes2023
Protective Renalase Deficiency in β-Cells Shapes Immune Metabolism and Function in Autoimmune Diabetes.
Article in Diabetes, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Single-gene knockout of RNLS or HIVEP2 are insufficient to protect β-cell spheroids from allo- and xeno-rejection.Frontiers in immunology · 2026Article
- Renalase inhibition defends against acute and chronic β cell stress by regulating cell metabolism.Molecular metabolism · 2025Article
- Renalase alleviates salt-induced kidney necroptosis and inflammation.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Article
- Renalase protects against podocyte injury by inhibiting oxidative stress and apoptosis in diabetic nephropathy.Open life sciences · 2024Article
- Beta cells deficient forFrontiers in immunology · 2024Article
- β Cell Stress and Endocrine Function During T1D: What Is Next to Discover?Endocrinology · 2023Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Type 1 diabetes (T1D) is caused by the immune-mediated loss of pancreatic β-cells that produce insulin. The latest advances in stem cell (SC) β-cell differentiation methods have made a cell replacement therapy for T1D feasible. However, recurring autoimmunity would rapidly destroy transplanted SC β-cells. A promising strategy to overcome immune rejection is to genetically engineer SC β-cells. We previously identified Renalase (Rnls) as a novel target for β-cell protection. Here we show that Rnls deletion endows β-cells with the capacity to modulate the metabolism and function of immune cells within the local graft microenvironment. We used flow cytometry and single-cell RNA sequencing to characterize β-cell graft-infiltrating immune cells in a mouse model for T1D. Loss of Rnls within transplanted β-cells affected both the composition and the transcriptional profile of infiltrating immune cells in favor of an anti-inflammatory profile with decreased antigen-presenting capacity. We propose that changes in β-cell metabolism mediate local immune regulation and that this feature could be exploited for therapeutic goals. ARTICLE HIGHLIGHTS: Protective Renalase (Rnls) deficiency impacts β-cell metabolism. Rnls-deficient β-cell grafts do not exclude immune infiltration. Rnls deficiency in transplanted β-cells broadly modifies local immune function. Immune cell in Rnls mutant β-cell grafts adopt a noninflammatory phenotype.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.