ArticleMolecular therapy : the journal of the American Society of Gene Therapy2023
Asparagine endopeptidase protects podocytes in adriamycin-induced nephropathy by regulating actin dynamics through cleaving transgelin.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 14 citations in OpenAlex.
- Molecular mechanisms and novel therapeutic targets of diabetic kidney disease.Chinese medical journal · 2026Review
- High-fat diet leads to male reproductive dysfunction by disrupting lipid-droplet-mediated organelle crosstalk.Cellular & molecular biology letters · 2026Article
- Glomerular cell atlas of multi-disease model revealed the characteristic changes of glomerular cell subtypes in diseases.Frontiers in immunology · 2026Article
- Validation and Evaluation of SPP1 as a Candidate Biomarker for Disease Monitoring in Focal Segmental Glomerulosclerosis.International journal of nephrology and renovascular disease · 2026Article
- Vincristine Treatment Protects Against Podocyte Damage in Focal Segmental Glomerulosclerosis.Kidney international reports · 2025Article
- Podocyte FFAR4 deficiency aggravated glomerular diseases and aging.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- PRDM16 deficiency promotes podocyte injury by impairing insulin receptor signaling.Cell death and differentiation · 2025Article
- SA4503 Mitigates Adriamycin-Induced Nephropathy via Sigma-1 Receptor in Animal and Cell-Based Models.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Human Adipose Tissue-Derived Stromal Cells Ameliorate Adriamycin-Induced Nephropathy by Promoting Angiogenesis.Organogenesis · 2024Article
- Cytoskeleton Rearrangement in Podocytopathies: An Update.International journal of molecular sciences · 2024Review
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9 authors at 2 institutions in 1 country.
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Abstract
Focal segmental glomerulosclerosis (FSGS) is the most common glomerular disorder causing end-stage renal diseases worldwide. Central to the pathogenesis of FSGS is podocyte dysfunction, which is induced by diverse insults. However, the mechanism governing podocyte injury and repair remains largely unexplored. Asparagine endopeptidase (AEP), a lysosomal protease, regulates substrates by residue-specific cleavage or degradation. We identified the increased AEP expression in the primary proteinuria model which was induced by adriamycin (ADR) to mimic human FSGS. In vivo, global AEP knockout mice manifested increased injury-susceptibility of podocytes in ADR-induced nephropathy (ADRN). Podocyte-specific AEP knockout mice exhibited much more severe glomerular lesions and podocyte injury after ADR injection. In contrast, podocyte-specific augmentation of AEP in mice protected against ADRN. In vitro, knockdown and overexpression of AEP in human podocytes revealed the cytoprotection of AEP as a cytoskeleton regulator. Furthermore, transgelin, an actin-binding protein regulating actin dynamics, was cleaved by AEP, and, as a result, removed its actin-binding regulatory domain. The truncated transgelin regulated podocyte actin dynamics and repressed podocyte hypermotility, compared to the native full-length transgelin. Together, our data reveal a link between lysosomal protease AEP and podocyte cytoskeletal homeostasis, which suggests a potential therapeutic role for AEP in proteinuria disease.
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