ArticleACS omega2025
Klotho Suppresses Indoxyl Sulfate-Mediated Apoptosis in Human Kidney Proximal Tubular (HK-2) Cells through Modulating the AKT/Nrf2 Mechanism.
Article in ACS omega, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The trial behind it
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Who cites it
7 citing papers in PubMed.
- Trained Immunity as a Mechanistic Bridge Between Uremic Toxins, Atherosclerosis, and Vascular Calcification in Chronic Kidney Disease.Cardiovascular toxicology · 2026Review
- Shaping death: how the microbiome regulates tumour cell demise and therapy response.Cancer metastasis reviews · 2026Review
- Indoxyl sulfate in the gut-kidney axis: from diet-microbiome interactions to renal injury and targeted therapies.Frontiers in nutrition · 2026Review
- The gut-kidney axis in chronic kidney disease: a vicious cycle of microbial dysbiosis and uremic toxin accumulation.Frontiers in immunology · 2026Review
- Fetuin-A and Heme Oxygenase 1 as Potential New Markers in the Diagnosis of Diabetic Kidney Disease.International journal of molecular sciences · 2025Review
- The Non-Traditional Cardiovascular Culprits in Chronic Kidney Disease: Mineral Imbalance and Uremic Toxin Accumulation.International journal of molecular sciences · 2025Review
- Astaxanthin activates the Nrf2/HO-1 pathway to attenuate indoxyl sulfate-induced oxidative stress and DNA damage in renal tubular epithelial cells.Frontiers in pharmacology · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic kidney disease (CKD) is a progressive condition with substantial prevalence worldwide. The uremic toxin indoxyl sulfate (IS) is known to induce tubulotoxicity and adverse effects in various organs. It has been shown that the expression of the antiaging klotho protein is downregulated in the IS-stimulated proximal tubule cells and kidneys, but the detailed mechanism underlying the implication of reduced klotho in nephropathy remains largely unclear. In the present study, we demonstrated that the repressed klotho following IS stimulation contributed to the reduced cell viability and increased cytotoxicity of HK-2 cells (a proximal tubular cell line). We showed that recombinant klotho reversed the AKT/Nrf2 axis in the IS-treated HK-2 cells, leading to the restoration of the antioxidant HO-1, NQO1, and SOD as well as diminished ROS production. Most importantly, our results suggested that the IS-induced alteration of mitochondrial membrane potential, mitochondrial COX-III mRNA expression, and mitochondrial complex III activity was all mediated by the klotho/AKT/Nrf2 axis. By examining the expression of Bax, Bcl-2, and cytochrome
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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 OpenQuestion graph.