ArticleThe Kaohsiung journal of medical sciences2024
Complement factor B inhibitor LNP023 mediates the effect and mechanism of AMPK/mTOR on autophagy and oxidative stress in lupus nephritis.
Article in The Kaohsiung journal of medical sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Hepatocyte SLC31A1-dependent copper accumulation contributes to hepatic glucose and lipid metabolic disturbances through AMPKα1 inactivation.Biochemistry and biophysics reports · 2026Article
- Identification and validation of key autophagy-related genes in Lupus nephritis.Clinical rheumatology · 2026Article
- Global perspectives on lupus nephritis: a review of clinical trials and therapeutic innovations.Frontiers in immunology · 2026Review
- Combined Network Pharmacology, Transcriptomics and Metabolomics Strategies Reveal the Mechanism of Action of Lang Chuang Wan to Ameliorate Lupus Nephritis in MRL/lpr Mice.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Complement factor B inhibitor LNP023 mediates the effect and mechanism of AMPK/mTOR on autophagy and oxidative stress in lupus nephritis.The Kaohsiung journal of medical sciences · 2024Article
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4 authors.
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Abstract
This study investigated the impact of LNP023 on the AMPK/mTOR signaling pathway in lupus nephritis (LN) and its effects on autophagy and oxidative stress. A mouse model of LN was established, and renal injury was confirmed by assessing various LN markers, including antinuclear antibody, ds-DNA, anti-Sm antibody, and others. Mice were treated with LNP023, the AMPK activator AICAR, or the AMPK inhibitor dorsomorphin. Renal injury and fibrosis were evaluated using HE and Masson staining. Expression levels of AMPK, mTOR, LC3, Beclin1, and p62 were assessed by immunohistochemistry and Western blot. Oxidative stress and inflammatory markers were measured by polymerase chain reaction and enzyme-linked immunosorbent assay. LN mice exhibited low AMPK/p-AMPK and high mTOR/p-mTOR levels, alongside significant renal injury, fibrosis, reduced autophagy, and elevated oxidative stress. LNP023 treatment improved these parameters, with enhanced effects when combined with AICAR. Conversely, dorsomorphin reversed LNP023's therapeutic benefits. The complement factor B inhibitor LNP023 promotes kidney health in LN mice by mediating the AMPK/mTOR pathway, promoting autophagy, and attenuating oxidative stress.
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