{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,31]],"date-time":"2026-07-31T23:54:14Z","timestamp":1785542054483,"version":"3.56.0"},"reference-count":45,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"7","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2017,7]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Chronic kidney disease (\n              <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\n              ) increases the occurrence of atrial fibrillation and pulmonary vein (\n              <jats:styled-content style=\"fixed-case\">PV<\/jats:styled-content>\n              ) arrhythmogenesis. Calcium dysregulation and reactive oxygen species (\n              <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content>\n              ) enhance\n              <jats:styled-content style=\"fixed-case\">PV<\/jats:styled-content>\n              arrhythmogenic activity. The purposes of this study were to investigate whether\n              <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\n              modulates\n              <jats:styled-content style=\"fixed-case\">PV<\/jats:styled-content>\n              electrical activity through dysregulation of calcium homeostasis and\n              <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content>\n              .\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Biochemical and electrocardiographic studies were conducted in rabbits with and without\n              <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\n              (induced by 150\u00a0mg\/kg per day neomycin sulfate and 500\u00a0mg\/kg per day cefazolin). Confocal microscopy with fluorescence and a whole\u2010cell patch clamp were applied to study calcium homeostasis and electrical activities in control and\n              <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\n              isolated single\n              <jats:styled-content style=\"fixed-case\">PV<\/jats:styled-content>\n              cardiomyocytes with or without treatment with H89 (1\u00a0\u03bcmol\/L, a protein kinase A inhibitor) and MPG (N\u2010[2\u2010mercaptopropionyl]glycine; 100\u00a0\u03bcmol\/L, a\n              <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content>\n              scavenger). The\n              <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content>\n              in mitochondria and cytosol were evaluated via intracellular dye fluorescence and lipid peroxidation.\n              <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\n              rabbits had excessive atrial premature captures over those of control rabbits. Compared with the control,\n              <jats:styled-content style=\"fixed-case\">CKD PV<\/jats:styled-content>\n              cardiomyocytes had a faster beating rate and larger calcium transient amplitudes, sarcoplasmic reticulum calcium contents, sodium\/calcium exchanger currents, and late sodium currents but smaller L\u2010type calcium current densities.\n              <jats:styled-content style=\"fixed-case\">CKD PV<\/jats:styled-content>\n              cardiomyocytes had a higher frequency and longer duration of calcium sparks and more\n              <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content>\n              in the mitochondria and cytosol than did controls. Moreover, H89 suppressed all calcium sparks in\n              <jats:styled-content style=\"fixed-case\">CKD PV<\/jats:styled-content>\n              cardiomyocytes, and H89\u2010 and\n              <jats:styled-content style=\"fixed-case\">MPG<\/jats:styled-content>\n              \u2010treated\n              <jats:styled-content style=\"fixed-case\">CKD PV<\/jats:styled-content>\n              cardiomyocytes had similar calcium transients compared with control\n              <jats:styled-content style=\"fixed-case\">PV<\/jats:styled-content>\n              cardiomyocytes.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>\n              increases\n              <jats:styled-content style=\"fixed-case\">PV<\/jats:styled-content>\n              arrhythmogenesis with enhanced calcium\u2010handling abnormalities through activation of protein kinase A and\n              <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content>\n              .\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.117.005701","type":"journal-article","created":{"date-parts":[[2017,7,13]],"date-time":"2017-07-13T00:10:32Z","timestamp":1499904632000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":21,"title":["Redox and Activation of Protein Kinase A Dysregulates Calcium Homeostasis in Pulmonary Vein Cardiomyocytes of Chronic Kidney Disease"],"prefix":"10.1161","volume":"6","author":[{"given":"Shih\u2010Yu","family":"Huang","sequence":"first","affiliation":[{"name":"Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan"},{"name":"Division of Cardiology, Department of Internal Medicine, Cathay General Hospital, Taipei, Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yao\u2010Chang","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Biomedical Engineering, National Defense Medical Center, Taipei, Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yu\u2010Hsun","family":"Kao","sequence":"additional","affiliation":[{"name":"Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan"},{"name":"Department of Medical Education and Research, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ming\u2010Hsiung","family":"Hsieh","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan"},{"name":"Division of Cardiovascular Medicine, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yung\u2010Kuo","family":"Lin","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan"},{"name":"Division of Cardiovascular Medicine, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shih\u2010Ann","family":"Chen","sequence":"additional","affiliation":[{"name":"School of Medicine, National Yang\u2010Ming University, Taipei, Taiwan"},{"name":"Division of Cardiology and Cardiovascular Research Center, Veterans General Hospital\u2010Taipei, Taipei, Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yi\u2010Jen","family":"Chen","sequence":"additional","affiliation":[{"name":"Graduate Institute of Clinical Medicine, College of 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