Lupus & antiphospholipid syndrome
Interferon α-induced HERC6 provokes podocyte dysfunction via mitotic catastrophe in lupus nephritis
Authors' conclusion
This study unveiled a novel pathway wherein HERC6 induced podocyte injury through disruption of mitotic homeostasis, revealed its potential as a therapeutic target in LN.
Study context
- Population
- Lupus nephritis (LN) patients, two lupus murine models (MRL/lpr mice) and podocytes in vitro
- Comparison
- Renal HERC6 knockdown vs control in MRL/lpr mice and IFN-α-stimulated podocytes
- Outcome
- Role and mechanism of HERC6 in podocyte injury of LN
Methodological detailsbioinformatic screening, LN patient renal tissue and urine, two lupus murine models, AAV9-mediated renal HERC6 knockdown in MRL/lpr mice, in vitro IFN-α-stimulated podocytes
- Bioinformatic screening
- LN patient renal tissue and urine
- Two lupus murine models
- AAV9-mediated renal HERC6 knockdown in MRL/lpr mice
- In vitro IFN-α-stimulated podocytes
Main finding
As reported in the abstract
- HERC6 identified as a key differentially expressed gene in LN
- HERC6 significantly upregulated in renal tissues, especially glomerulus, of LN patients and two murine lupus models
- Urinary HERC6 significantly elevated in LN patients, correlated tightly with disease activity indicators incl. proteinuria and hypocomplementemia
- Renal-targeted HERC6 knockdown significantly attenuated LN progression and alleviated podocyte injury in MRL/lpr mice
- IFN-α directly induced HERC6 expression in podocytes
- HERC6 knockdown markedly alleviated IFN-α-induced podocyte injury: restored podocyte markers, reduced inflammatory cytokine secretion, decreased apoptosis
- HERC6 deficiency reversed IFN-α-induced mitotic spindle abnormalities and G2/M phase arrest
Original publication
Interferon α-induced HERC6 provokes podocyte dysfunction via mitotic catastrophe in lupus nephritis. Arthritis Res Ther. Published 22 April 2026. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →