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ABSTRACT: Background
IgA nephropathy (IgAN) is the most common primary GN worldwide. Circulating immune complexes form that are prone to deposition in the mesangium, where they trigger glomerular inflammation. A growing body of evidence suggests that dysregulated expression of microRNAs in IgAN may play a significant role in establishing the disease phenotype.Methods
We generated single miR-23b-3p(miR-23b) knockout mice using CRISPR-Cas9.Results
In humans, miR-23b levels are downregulated in kidney biopsies and sera of patients with IgAN, and serum miR-23b levels are negatively correlated with serum IgA1 levels. We show that miR-23b-/- mice develop an IgAN-like phenotype of mesangial IgA and C3 deposition associated with development of albuminuria, hypertension, an
SUBMITTER: Li H
PROVIDER: S-EPMC8722801 | biostudies-literature | 2021 Oct
REPOSITORIES: biostudies-literature