ArticleDrug design, development and therapy2026
Astragaloside IV Alleviates Lupus Nephritis by Inhibiting Podocyte Ferroptosis via the PI3K/AKT/Nrf2 Pathway.
Article in Drug design, development and therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Lupus nephritis (LN) is an immune complex-mediated glomerulonephritis caused by systemic lupus erythematosus (SLE) involving the kidneys. Astragaloside IV (AS-IV) is the main active ingredient of the traditional Chinese medicine Astragalus membranaceus, belonging to the cycloartane-type triterpenoid saponins, and has anti-inflammatory and antioxidant pharmacological effects. This study mainly explores the therapeutic potential and molecular mechanism of AS-IV for LN. Methods: Using MRL/lpr mice as an in vivo model, the effects of AS-IV on the histopathology and ultrastructure of renal tissues were evaluated by histopathological staining and transmission electron microscopy (TEM). Immunofluorescence and biochemical kits were used to assess the changes in renal damage indicators. Network pharmacology and molecular docking were employed to reveal the molecular targets of AS-IV in the intervention of lupus nephritis (LN). In vitro, a puromycin aminonucleoside (PAN)-induced ferroptosis model of MPC-5 cells was established to evaluate the effects of AS-IV on ferroptosis and the PI3K/AKT/Nrf2 pathway in MPC-5 cells, and further verification was carried out through rescue experiments. Results: AS-IV can improve the renal histopathology of MRL/lpr mice, reduce the glomerular score, perivascular wall score, foot process fusion rate, and electron-dense deposit density, and decrease the levels of 24hPRO, UTPCR, and UACR, showing a certain protective effect on the kidneys. Meanwhile, AS-IV can upregulate the damage-related proteins in MPC-5 cells, increase the levels of factors related to the PI3K/AKT/Nrf2 pathway, GPX4, SLC7A11, DHODH, FSP1, GSH, and SOD in MPC-5 cells, and reduce the levels of Fe Conclusion: AS-IV can inhibit podocyte ferroptosis by regulating the PI3K/AKT/Nrf2 axis, reduce the degree of kidney damage, and thus relieve LN. This also indicates that AS-IV has certain therapeutic potential in the treatment of LN.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.