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Article Abstract
Genetically induced decay-accelerating factor (DAF) overexpression prevents adriamycin (ADR)-induced focal segmental glomerulosclerosis (FSGS) in mice. Pharmacologic inhibition of DAF cleavage reduces complement activation in the glomeruli and albuminuria in murine ADR-induced FSGS. Inhibition of complement activation represents a valuable therapeutic strategy for FSGS and, potentially, other glomerular diseases.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10103208 | PMC |
| http://dx.doi.org/10.34067/KID.0005312022 | DOI Listing |
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