ArticleScientific reports2021
Artemether ameliorates kidney injury by restoring redox imbalance and improving mitochondrial function in Adriamycin nephropathy in mice.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Construction of an activatable ratiometric fluorescent nanoprobe for HClO detection and imaging in acute kidney injury models.RSC advances · 2026Article
- Biallelic BRF2 mutations disrupt redox homeostasis as etiological factors in syndromic immunodeficiency and developmental disorders.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Activation of sirtuin 3 and maintenance of mitochondrial homeostasis by artemisinin protect against diclofenac-induced kidney injury in rats.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Artemisinin and Its Derivatives: Promising Therapeutic Agents for Age-Related Macular Degeneration.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Mitochondrial pyruvate carrier 2 mitigates acute kidney injury via sustaining mitochondrial metabolism.International journal of biological sciences · 2024Article
- Artemether regulates liver glycogen and lipid utilization through mitochondrial pyruvate oxidation in db/db mice.American journal of translational research · 2024Article
- Artemether ameliorates adriamycin induced cardiac atrophy in mice.Molecular medicine reports · 2023Article
- Therapeutic potential of artemisinin and its derivatives in managing kidney diseases.Frontiers in pharmacology · 2023Review
- Roles of Mitochondrial DNA Damage in Kidney Diseases: A New Biomarker.International journal of molecular sciences · 2022Review
- Artemether attenuates renal tubular injury by regulating iron metabolism in mice with streptozotocin-induced diabetes.American journal of translational research · 2022Article
- Artemether attenuates renal tubular injury by targeting mitochondria in adriamycin nephropathy mice.American journal of translational research · 2022Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The kidney is a high-energy demand organ rich in mitochondria especially renal tubular cells. Emerging evidence suggests that mitochondrial dysfunction, redox imbalance and kidney injury are interconnected. Artemether has biological effects by targeting mitochondria and exhibits potential therapeutic value for kidney disease. However, the underlying molecular mechanisms have not been fully elucidated. This study was performed to determine the effects of artemether on Adriamycin-induced nephropathy and the potential mechanisms were also investigated. In vivo, an Adriamycin nephropathy mouse model was established, and mice were treated with or without artemether for 2 weeks. In vitro, NRK-52E cells were stimulated with TGF-β1 and treated with or without artemether for 24 h. Then renal damage and cell changes were evaluated. The results demonstrated that artemether reduced urinary protein excretion, recovered podocyte alterations, attenuated pathological changes and alleviated renal tubular injury. Artemether also downregulated TGF-β1 mRNA expression levels, inhibited tubular proliferation, restored tubular cell phenotypes and suppressed proliferation-related signalling pathways. In addition, artemether restored renal redox imbalance, increased mtDNA copy number and improved mitochondrial function. In summary, we provided initial evidence that artemether ameliorates kidney injury by restoring redox imbalance and improving mitochondrial function in Adriamycin nephropathy in mice. Artemether may be a promising agent for the treatment kidney disease.
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