{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:09:13Z","timestamp":1787015353691,"version":"build-2736575974"},"reference-count":39,"publisher":"Wiley","issue":"15","license":[{"start":{"date-parts":[[2020,7,8]],"date-time":"2020-07-08T00:00:00Z","timestamp":1594166400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100012553","name":"Chang Gung Memorial Hospital","doi-asserted-by":"crossref","award":["CMRPG8F1311"],"award-info":[{"award-number":["CMRPG8F1311"]}],"id":[{"id":"10.13039\/100012553","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2020,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Increased circulating level of uraemic solute p\u2010cresyl 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\u00a0\u00b5g\/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\u00a0\u00b5g\/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\u2010sensing adenosine monophosphate\u2010activated 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\u2010level PCS not only caused AMPK\u2010dependent mitochondrial hyperfusion but also induced cell enlargement in H9C2 cardiomyoblasts in vitro.<\/jats:p>","DOI":"10.1111\/jcmm.15303","type":"journal-article","created":{"date-parts":[[2020,7,8]],"date-time":"2020-07-08T08:41:37Z","timestamp":1594197697000},"page":"8379-8390","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["P\u2010cresyl sulfate causes mitochondrial hyperfusion in H9C2 cardiomyoblasts"],"prefix":"10.1111","volume":"24","author":[{"given":"Tien\u2010Hung","family":"Huang","sequence":"first","affiliation":[{"name":"Division of Cardiology Department of Internal Medicine Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine Kaohsiung Taiwan"},{"name":"Institute for Translational Research in Biomedicine Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College 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