ArticleCell death & disease2023
Minnelide combined with anti-ANGPTL3-FLD monoclonal antibody completely protects mice with adriamycin nephropathy by promoting autophagy and inhibiting apoptosis.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.
- Genetic association analysis of lipid-lowering drug target genes in chronic kidney disease.Frontiers in endocrinology · 2024Pooled it
- Review
- Anti-ANGPTL3 antibody and IL-22 fusion protein mitigate nephrotic syndrome via mitochondrial protection, anti-apoptosis, and autophagy suppression.Antibody therapeutics · 2026Article
- Urinary ANGPTL3: a novel noninvasive biomarker for podocyte injury in pediatric glomerular diseases.Journal of translational medicine · 2026Article
- Targeting angiopoietin-like protein 3 and interleukin-1β alleviated liver and kidney injury through attenuation of lipotoxicity and regulation of glycolipid metabolism in db/db mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Minnelide ameliorates Col4a5+/- mice by upregulating Col4a5 and alleviating endoplasmic reticulum stress.Frontiers in pharmacology · 2026Article
- A CPEB2/ANGPTL3 feedback loop promotes the progression of podocyte injury in nephrotic syndrome.Scientific reports · 2025Article
- Behavioral Abnormalities, Cognitive Impairments, Synaptic Deficits, and Gene Replacement Therapy in a CRISPR Engineered Rat Model of 5p15.2 Deletion Associated With Cri du Chat Syndrome.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Cold and hot tumors: from molecular mechanisms to targeted therapy.Signal transduction and targeted therapy · 2024Review
- Enzyme-activatable kidney-targeted dendrimer-drug conjugate for efficient childhood nephrotic syndrome therapy.Theranostics · 2024Article
- Shensu IV maintains the integrity of the glomerular filtration barrier and exerts renal protective effects by regulating endogenous hydrogen sulfide levels.Frontiers in pharmacology · 2024Article
- Research Progress of Triptolide Against Fibrosis.Drug design, development and therapy · 2024Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Minimal change disease (MCD) is the common type of nephrotic syndrome (NS) in children. Currently, there is an urgent need to explore new treatments because of the significant side effects of long-term use of glucocorticoids and immunosuppressive drugs and the failure to reduce proteinuria in some patients. Angiopoietin-like protein 3 (Angptl3) is an essential target of NS, and anti-ANGPTL3-FLD monoclonal antibody (mAb) significantly reduces proteinuria in mice with adriamycin nephropathy (AN). However, some proteinuria is persistent. Minnelide, a water-soluble prodrug of triptolide, has been used for the treatment of glomerular disease. Therefore, the present study aimed to investigate whether minnelide combined with mAb could further protect mice with AN and the underlying mechanisms. 8-week-old C57BL/6 female mice were injected with 25 mg/kg of Adriamycin (ADR) by tail vein to establish the AN model. A dose of 200 μg/kg of minnelide or 20 mg/kg of mAb was administered intraperitoneally for the treatment. In vitro, the podocytes were treated with 0.4 μg/mL of ADR for 24 h to induce podocyte injury, and pretreatment with 10 ng/mL of triptolide for 30 min or 100 ng/mL of mAb for 1 h before ADR exposure was used to treat. The results showed that minnelide combined with mAb almost completely ameliorates proteinuria and restores the ultrastructure of the podocytes in mice with AN. In addition, minnelide combined with mAb restores the distribution of Nephrin, Podocin, and CD2AP and reduces the level of inflammatory factors in mice with AN. Mechanistically, minnelide combined with mAb could further alleviate apoptosis and promote autophagy in mice with AN by inhibiting the mTOR signaling pathway. In vitro, triptolide combined with mAb increases the expression of Nephrin, Podocin, and CD2AP, alleviates apoptosis, and promotes autophagy. Overall, minnelide combined with mAb completely protects the mice with AN by promoting autophagy and inhibiting apoptosis.
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