Search Results - "Kim, Maengjo"

Defective Branched-Chain Amino Acid Catabolism Disrupts Glucose Metabolism and Sensitizes the Heart to Ischemia-Reperfusion Injury by Li, Tao, Zhang, Zhen, Kolwicz, Stephen C., Abell, Lauren, Roe, Nathan D., Kim, Maengjo, Zhou, Bo, Cao, Yang, Ritterhoff, Julia, Gu, Haiwei, Raftery, Daniel, Sun, Haipeng, Tian, Rong

“…Elevated levels of branched-chain amino acids (BCAAs) have recently been implicated in the development of cardiovascular and metabolic diseases, but the…”
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Activation of γ2-AMPK Suppresses Ribosome Biogenesis and Protects Against Myocardial Ischemia/Reperfusion Injury by Cao, Yang, Bojjireddy, Naveen, Kim, Maengjo, Li, Tao, Zhai, Peiyong, Nagarajan, Narayani, Sadoshima, Junichi, Palmiter, Richard D, Tian, Rong

“…RATIONALE:AMP-activated protein kinase (AMPK) is a heterotrimeric protein that plays an important role in energy homeostasis and cardioprotection. Two isoforms…”
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Preservation of myocardial fatty acid oxidation prevents diastolic dysfunction in mice subjected to angiotensin II infusion by Choi, Yong Seon, MD, PhD, de Mattos, Ana Barbosa Marcondes, PhD, Shao, Dan, PhD, Li, Tao, PhD, Nabben, Miranda, PhD, Kim, Maengjo, PhD, Wang, Wang, MD, PhD, Tian, Rong, MD, PhD, Kolwicz, Stephen C., PhD

“…Abstract Rationale Diastolic dysfunction is a common feature in many heart failure patients with preserved ejection fraction and has been associated with…”
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AMPK isoform expression in the normal and failing hearts by Kim, Maengjo, Shen, Mei, Ngoy, Soeun, Karamanlidis, Georgios, Liao, Ronglih, Tian, Rong

“…Abstract AMP-activated protein kinase (AMPK) is a master metabolic switch that plays an important role in energy homeostasis at the cellular and whole body…”
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Mutation in the γ2-Subunit of AMP-Activated Protein Kinase Stimulates Cardiomyocyte Proliferation and Hypertrophy Independent of Glycogen Storage by Kim, Maengjo, Hunter, Roger W, Garcia-Menendez, Lorena, Gong, Guohua, Yang, Yu-Ying, Kolwicz, Stephen C, Xu, Jason, Sakamoto, Kei, Wang, Wang, Tian, Rong

“…RATIONALE:AMP-activated protein kinase is a master regulator of cell metabolism and an attractive drug target for cancer and metabolic and cardiovascular…”
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Role of resistin in cardiac contractility and hypertrophy by Kim, Maengjo, Oh, Jae kyun, Sakata, Susumu, Liang, Iifan, Park, WooJin, Hajjar, Roger J, Lebeche, Djamel

“…Abstract Cardiovascular sequelae including diabetic cardiomyopathy constitute the major cause of death in diabetic patients. Although several factors may…”
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TFEB Overexpression, Not mTOR Inhibition, Ameliorates RagCS75Y Cardiomyopathy by Kim, Maengjo, Lu, Linghui, Dvornikov, Alexey V., Ma, Xiao, Ding, Yonghe, Zhu, Ping, Olson, Timothy M., Lin, Xueying, Xu, Xiaolei

“…A de novo missense variant in Rag GTPase protein C (RagCS75Y) was recently identified in a syndromic dilated cardiomyopathy (DCM) patient. However, its…”
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Gene remodeling in type 2 diabetic cardiomyopathy and its phenotypic rescue with SERCA2a by Karakikes, Ioannis, Kim, Maengjo, Hadri, Lahouaria, Sakata, Susumu, Sun, Yezhou, Zhang, Weijia, Chemaly, Elie R, Hajjar, Roger J, Lebeche, Djamel

“…Diabetes-associated myocardial dysfunction results in altered gene expression in the heart. We aimed to investigate the changes in gene expression profiles…”
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Targeting AMPK for cardiac protection: Opportunities and challenges by Kim, Maengjo, Tian, Rong

“…Abstract AMP-activated protein kinase (AMPK) regulates cellular energy homeostasis and multiple biological processes in cell growth and survival, hence an…”
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Abstract 11556: Sodium/Glucose Co-Transporter 2 Inhibition and Attenuation of the Action Potential Duration in Patient-Specific Re-Engineered Heart Cells With Congenital Long QT Syndrome by Zhou, Wei, Kim, Maengjo, Tester, David J, Giudicessi, John, Ackerman, Michael J

“…BackgroundLong QT syndrome (LQTS) stems from cardiac action potential duration (APD) prolonging pathogenic variants in KCNQ1 (LQT1), KCNH2 (LQT2), or SCN5A…”
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Abstract 10986: SGK1 Inhibition Attenuated the Action Potential Duration In-Patient and Genotype-Specific Re-Engineered Heart Cells With Congenital Long QT Syndrome by Tester, David J, Das, Saumya, Kim, Maengjo, Pradhananga, Sabindra, Hamrick, Samantha K, Srinivasan, Dinesh, Sager, Philip, Ackerman, Michael J

“…BackgroundLong QT syndrome (LQTS) often stems from pathogenic variants in KCNQ1 (LQT1), KCNH2 (LQT2), or SCN5A (LQT3) and is characterized cellularly by…”
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Abstract 11027: SGK1 Inhibition and Attenuation of the Action Potential Duration in Re-Engineered Heart Cell Models of Drug-Induced QT Prolongation by Tester, David J, Sager, Philip T, Kim, Maengjo, Pradhananga, Sabindra, Hamrick, Samantha K, Srinivasan, Dinesh, Das, Saumya, Ackerman, Michael J

“…BackgroundDrug-induced QT prolongation (DI-QTP) is a clinical entity in which administration of a HERG/IKr blocker such as dofetilide prolongs the cardiac…”
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BS-513-01 SUPPRESSION-REPLACEMENT GENE THERAPY FOR SCN5A-MEDIATED TYPE 3 LONG QT SYNDROME by Gluscevic, Martina, Kim, Changsung John, Tester, David, Kim, Maengjo, Bains, Sahej, Ackerman, Michael John

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PO-646-04 FUNCTIONAL CHARACTERIZATION AND IDENTIFICATION OF A THERAPEUTIC FOR A NOVEL SCN5A-F1760C VARIANT CAUSING TYPE 3 LONG QT SYNDROME REFRACTORY TO ALL GUIDELINE DIRECTED THERAPIES by Stutzman, Marissa Joy, Kim, Maengjo, Ye, Dan, Tester, David, Shannon, Kevin M., Ackerman, Michael John

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Abstract 446: Transcription Factor EB, Not mTOR is a Therapeutic Target for Rag GTPase Protein C S75Y-based Cardiomyopathy by Kim, Maengjo, Qi, Qiu, Ma, Xiao, Xu, Xiaolei

“…Abstract only Rationale: We recently reported the association of S75Y, a point mutation in the Rag GTPase protein C ( RRAGC ) gene, with pediatric DCM. Because…”
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Transcript variant dictates Prkag2 cardiomyopathy? by Kim, Maengjo, Tian, Rong

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Abstract 10669: Phenytoin, an Anti-Epileptic Sodium Channel Blocker, May Be a Novel Therapy for Type 3 Long Qt Syndrome Mediated by the Lidocaine-Insensitive SCN5A-F1760C Variant by Ye, Dan, Stutzman, Marissa, Kim, Maengjo, Gluscevic, Martina, Zhou, Wei, Gao, Xiaozhi, Tester, David J, Giudicessi, John, Shannon, Kevin, Ackerman, Michael J

“…IntroductionGain-of-function mutations in SCN5A-encoded cardiac sodium channel (NaV1.5) cause type 3 long QT syndrome (LQT3). Patients with SCN5A variants…”
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B-PO01-007 THE EFFICACY OF MEXILETINE TREATMENT IN PATIENT-SPECIFIC RE-ENGINEERED CARDIOMYOCYTE MODELS OF LONG QT SYNDROME TYPE 1, 2, AND 3 by Gao, Xiaozhi, Kim, Maengjo, Zhou, Wei, Hamrick, Samantha K., John Kim, Changsung, Tester, David, Ackerman, Michael John

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Functional characterization and identification of a therapeutic for a novel SCN5A-F1760C variant causing type 3 long QT syndrome refractory to all guideline-directed therapies by Stutzman, Marissa J., Gao, Xiaozhi, Kim, Maengjo, Ye, Dan, Zhou, Wei, Tester, David J., Giudicessi, John R., Shannon, Kevin, Ackerman, Michael J.

“…Pathogenic variants in the SCN5A-encoded Nav1.5 sodium channel cause type 3 long QT syndrome (LQT3). We present the case of an infant with severe LQT3 who was…”
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SGK1 inhibition attenuates the action potential duration in reengineered heart cell models of drug-induced QT prolongation by Kim, Maengjo, Sager, Philip T., Tester, David J., Pradhananga, Sabindra, Hamrick, Samantha K., Srinivasan, Dinesh, Das, Saumya, Ackerman, Michael J.

“…Drug-induced QT prolongation (DI-QTP) is a clinical entity in which administration of a human ether-à-go-go–related gene/rapid delayed rectifier potassium…”
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