ArticleMolecular biology reports2023
Effects of honokiol protects against chronic kidney disease via BNIP3/NIX and FUNDC1-mediated mitophagy and AMPK pathways.
Article in Molecular biology reports, 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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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Pharmacological advances of honokiol: Mechanisms, targets and therapeutic potential (Review).Biomedical reports · 2026Review
- Review
- Mitophagy and oxidative stress in chronic kidney disease (Review).Molecular medicine reports · 2026Review
- Precision Nanomedicine for Renal Tubular Injury: From Passive Accumulation to Subcellular Targeting.International journal of nanomedicine · 2026Review
- Honokiol attenuates diabetic nephropathy by targeting SIRT3 to suppress mitochondrial ROS-induced pyroptosis.Diabetology & metabolic syndrome · 2025Article
- Exploring disulfiram mechanisms in renal fibrosis: insights from biological data and computational approaches.Frontiers in pharmacology · 2025Article
- Editorial: Identification of effective biomarkers for diagnosis and treatment of chronic kidney disease: integrating bioinformatics and pharmacological approaches.Frontiers in pharmacology · 2025Article
- Localization and Aggregation of Honokiol in the Lipid Membrane.Antioxidants (Basel, Switzerland) · 2024Article
- Multiple roles of mitochondrial autophagy receptor FUNDC1 in mitochondrial events and kidney disease.Frontiers in cell and developmental biology · 2024Review
- Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundChronic kidney disease (CKD) is a serious health threat worldwide. Defective mitophagy has been reported to induce mitochondrial dysfunction, which is closely associated with CKD pathogenesis. Honokiol (HKL) is a bioactive component of Magnolia officinalis that has multiple efficacies. Our study aimed to investigate the effect of HKL on a CKD rat model and explore the possible mechanisms of mitophagy mediated by Bcl-2 interacting protein 3 and BNIP3-like (NIX) (also known as the BNIP3/NIX pathway) and FUN14 domain-containing 1 (the FUNDC1 pathway) and the role of the AMP-activated protein kinase (AMPK) pathway.
methodsA CKD rat model was established by feeding the animals dietary adenine (0.75% w/w, 3 weeks). Simultaneously, the treatment group was given HKL (5 mg/kg/day, 4 weeks) by gavage. Renal function was assessed by measuring serum creatinine (Scr) and blood urea nitrogen (BUN) levels. Pathological changes were analyzed by periodic acid-Schiff (PAS) and Masson's trichrome staining. Protein expression was evaluated by Western blotting and immunohistochemistry.
resultsHKL treatment ameliorated the decline in renal function and reduced tubular lesions and interstitial fibrosis in CKD rats. Accordingly, the renal fibrosis markers Col-IV and α-SMA were decreased by HKL. Moreover, HKL suppressed the upregulation of the proapoptotic proteins Bad and Bax and Cleaved caspase-3 expression in CKD rats. Furthermore, HKL suppressed BNIP3, NIX and FUNDC1 expression, leading to the reduction of excessive mitophagy in CKD rats. Additionally, AMPK was activated by adenine, and HKL reversed this change and significantly decreased the level of activated AMPK (phosphorylated AMPK, P-AMPK).
conclusionHKL exerted a renoprotective effect on CKD rats, which was possibly associated with BNIP3/NIX and FUNDC1-mediated mitophagy and the AMPK pathway.
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