Key result
In human proximal tubular epithelial cells, IgA-activated mesangial cell mediators upregulated Ang II production, leading to inflammation via AT1R and subsequent apoptosis via AT2R.
In IgA nephropathy, Ang II receptor expression in proximal tubular epithelial cells is upregulated by mediators from IgA-activated mesangial cells, leading to inflammation and apoptosis.
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Should not change IgA nephropathy care; leaves open whether AT1R/AT2R modulation alters tubular injury or progression.
Chan et al. (2005) studied IgA nephropathy. Conditioned culture medium from human mesangial cells activated with IgA was evaluated on Expression and regulation of Ang II receptors and cellular responses. In human proximal tubular epithelial cells, IgA-activated mesangial cell mediators upregulated Ang II production, leading to inflammation via AT1R and subsequent apoptosis via AT2R.
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