Inhibition of RIPK1 kinase does not affect diabetes development: β-Cells survive RIPK1 activation.

ABSTRACT:

Objectives

Type 1 diabetes (T1D) is caused by progressive immune-mediated loss of insulin-producing β-cells. Inflammation is detrimental to β-cell function and survival, moreover, both apoptosis and necrosis have been implicated as mechanisms of F062-cell loss in T1D. The receptor interacting serine/threonine protein kinase 1 (RIPK1) promotes inflammation by serving as a scaffold for NF-F06BB and MAPK activation, or by acting as a kinase that triggers apoptosis or necroptosis. It is unclear whether RIPK1 kinase activity is involved in T1D pathology. In the present study, we investigated if absence of RIPK1 activation would affect the susceptibility to immune-mediated diabetes or diet induced obesity (DIO).

Methods

The RIPK1 knockin mouse line carrying a mutation mimicking se

SUBMITTER: Takiishi T 

PROVIDER: S-EPMC9932129 | biostudies-literature | 2023 Jan

REPOSITORIES: biostudies-literature