ArticleJournal of cellular and molecular medicine2020
P-cresyl sulfate causes mitochondrial hyperfusion in H9C2 cardiomyoblasts.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- Mechanistic pathways linking gut microbial metabolites, microbial structural products, and host-microbe co-metabolites to mitochondrial function.Gut microbes · 2026Pooled it
- Review
- Stress Induced Mitochondrial Hyperfusion (SIMH): A Concise Review on SIMH in Neurodegenerative Disorders and Other Diseases.Organelle (Tucson, Ariz.) · 2025Article
- SGLT2 inhibitor downregulated oxidative stress via activating AMPK pathway for cardiorenal (CR) protection in CR syndrome rodent fed with high protein diet.Journal of molecular histology · 2024Article
- The Molecular Mechanism and Therapeutic Strategy of Cardiorenal Syndrome Type 3.Reviews in cardiovascular medicine · 2023Review
- Role of the Gut Microbiome in Skeletal Muscle Physiology and Pathophysiology.Current osteoporosis reports · 2022Review
- The Role of Gut-Derived, Protein-Bound Uremic Toxins in the Cardiovascular Complications of Acute Kidney Injury.Toxins · 2022Review
- The Interplay between Uremic Toxins and Albumin, Membrane Transporters and Drug Interaction.Toxins · 2022Review
- Advances in Cardiotoxicity Induced by Altered Mitochondrial Dynamics and Mitophagy.Frontiers in cardiovascular medicine · 2021Review
- P-cresyl sulfate causes mitochondrial hyperfusion in H9C2 cardiomyoblasts.Journal of cellular and molecular medicine · 2020Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increased circulating level of uraemic solute p-cresyl sulphate (PCS) in patients with chronic kidney disease (CKD) is known to increase myocardial burden relevant to mitochondrial abnormalities. This study aimed at investigating mitochondrial response to PCS in H9C2 cardiomyoblasts. H9C2 cardiomyoblasts were treated with four different concentrations of PCS (3.125, 6.25, 12.5 and 25.0 µg/mL) to study the changes in cell proliferation, cell size and mitochondrial parameters including morphology, respiration, biogenesis and membrane potential. The lowest effective dose of PCS (6.25 µg/mL) induced mitochondrial hyperfusion with enhanced mitochondrial connectivity, mitochondrial oxygen consumption rates, mitochondrial mass, mitochondrial DNA copy number and increased volume of cardiomyoblasts. After PCS treatment, phosphorylation of energy-sensing adenosine monophosphate-activated protein kinase (AMPK) was increased without induction of apoptosis. In contrast, mitochondrial mass was recovered after AMPK silencing. Additionally, mitochondrial hyperfusion and cell volume were reversed after cessation of PCS treatment. The results of the present study showed that low-level PCS not only caused AMPK-dependent mitochondrial hyperfusion but also induced cell enlargement in H9C2 cardiomyoblasts in vitro.
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Registered trials
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