Dysfunctional β-cell autophagy induces β-cell stress and enhances islet immunogenicity.

ABSTRACT:

Background

Type 1 Diabetes (T1D) is caused by a combination of genetic and environmental factors that trigger autoimmune-mediated destruction of pancreatic β-cells. Defects in β-cell stress response pathways such as autophagy may play an important role in activating and/or exacerbating the immune response in disease development. Previously, we discovered that β-cell autophagy is impaired prior to the onset of T1D, implicating this pathway in T1D pathogenesis.

Aims

To assess the role of autophagy in β-cell health and survival, and whether defects in autophagy render islets more immunogenic.

Methods

We knocked out the critical autophagy enzyme, ATG7, in the β-cells of mice (ATG7^Δβ-cell) then monitored blood glucose, performed glucose tolerance tests, and eval

SUBMITTER: Austin MC 

PROVIDER: S-EPMC11814175 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature