Changwon Kho

ORCID: 0000-0001-7109-7506
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About
Contact & Profiles
Research Areas
  • Ubiquitin and proteasome pathways
  • Peptidase Inhibition and Analysis
  • Cardiac electrophysiology and arrhythmias
  • Cardiac Fibrosis and Remodeling
  • Cardiomyopathy and Myosin Studies
  • Pluripotent Stem Cells Research
  • Mitochondrial Function and Pathology
  • ATP Synthase and ATPases Research
  • Ion channel regulation and function
  • MicroRNA in disease regulation
  • RNA Interference and Gene Delivery
  • Cardiovascular Function and Risk Factors
  • Muscle Physiology and Disorders
  • Mechanical Circulatory Support Devices
  • Neuroscience and Neural Engineering
  • 3D Printing in Biomedical Research
  • Virus-based gene therapy research
  • Signaling Pathways in Disease
  • Connective Tissue Growth Factor Research
  • Cardiac Ischemia and Reperfusion
  • Circular RNAs in diseases
  • Viral Infections and Immunology Research
  • Genetics and Neurodevelopmental Disorders
  • Coenzyme Q10 studies and effects
  • Autophagy in Disease and Therapy

Pusan National University
2020-2024

Dunsan Korean Medicine Hospital
2024

Icahn School of Medicine at Mount Sinai
2011-2020

Cardiovascular Research Center
2009-2020

Changwon National University
2012-2016

Fondation pour l’innovation en Cadiométabolisme et Nutrition
2016

Pitié-Salpêtrière Hospital
2016

Sorbonne Université
2016

Assistance Publique – Hôpitaux de Paris
2016

Spanish National Centre for Cardiovascular Research
2014

Background: The adult mammalian heart has limited regenerative capacity, mostly attributable to postnatal cardiomyocyte cell cycle arrest. In the last 2 decades, numerous studies have explored regulatory mechanisms enhance myocardial regeneration after infarction. Pkm2 (Pyruvate kinase muscle isoenzyme 2) is an of glycolytic enzyme pyruvate kinase. role in proliferation, development, and cardiac unknown. Methods: We investigated effect cardiomyocytes through models loss...

10.1161/circulationaha.119.043067 article EN Circulation 2020-02-11

Abstract Decreased activity and expression of the cardiac sarcoplasmic reticulum calcium ATPase (SERCA2a), a critical pump regulating cycling in cardiomyocyte, are hallmarks heart failure. We have previously described role for small ubiquitin-like modifier type 1 (SUMO-1) as regulator SERCA2a shown that gene transfer SUMO-1 rodents large animal models failure restores function. Here, we identify characterize molecule, N106, which increases SUMOylation SERCA2a. This compound directly...

10.1038/ncomms8229 article EN cc-by Nature Communications 2015-06-12

Rationale: SERCA2a, sarco-endoplasmic reticulum Ca 2+ -ATPase, is a critical determinant of cardiac function. Reduced level and activity SERCA2a are major features heart failure. Accordingly, intensive efforts have been made to develop efficient modalities for activation. We showed that the enhanced by post-translational modification with SUMO1 (small ubiquitin-like modifier 1). However, roles other modifications on still unknown. Objective: In this study, we aim assess role lysine...

10.1161/circresaha.118.313865 article EN Circulation Research 2019-02-21

Recently, the impact of small ubiquitin-related modifier 1 (SUMO-1) on regulation and preservation sarcoplasmic reticulum calcium adenosine triphosphatase (SERCA2a) function was discovered. The amount myocardial SUMO-1 is decreased in failing hearts, its knockdown results severe heart failure (HF) mice. In a previous study, we showed that gene transfer substantially improved cardiac murine model pressure overload-induced HF. Toward clinical translation, evaluated this study effects swine...

10.1126/scitranslmed.3006487 article EN Science Translational Medicine 2013-11-13

Stromal interaction molecule 1 (STIM1) is a dynamic calcium signal transducer implicated in hypertrophic growth of cardiomyocytes. STIM1 thought to act as an initiator cardiac response at the level sarcolemma, but pathways underpinning this effect have not been examined.To determine mechanistic role hypertrophy and during transition heart failure, we manipulated expression mice cardiomyocytes by using vivo gene delivery specific short hairpin RNAs. In 3 different models, found that Stim1...

10.1161/circulationaha.115.020678 article EN Circulation 2016-04-11

Rationale: Abnormal SUMOylation has emerged as a characteristic of heart failure (HF) pathology. Previously, we found reduced SUMO1 (small ubiquitin-like modifier 1) expression and SERCA2a (sarcoplasmic reticulum Ca 2+ -ATPase) in human animal HF models. gene delivery or small molecule activation restored cardiac function Despite the critical role HF, regulatory mechanisms underlying are largely unknown. Objective: To examine miR-146a–mediated regulation its consequent effects on morphology...

10.1161/circresaha.118.312751 article EN Circulation Research 2018-08-31

Small ubiquitin-like modifier type 1 (SUMO-1) has been shown to play a critical role in the dysfunction of cardiac isoform sarcoplasmic reticulum calcium ATPase (SERCA2a) pump setting heart failure. In hypertrophy, SUMO-1 not defined and our study's goals were examine effects modulating on hypertrophic response both vitro vivo whether oxidative stress (during hypertrophy) is abrogated by gene transfer.In mice undergoing transverse aortic constriction (TAC), levels increased slightly during...

10.1089/ars.2014.5983 article EN Antioxidants and Redox Signaling 2014-06-03

MicroRNAs are promising therapeutic targets, because their inhibition has the potential to normalize gene expression in diseased states. Recently, our group found that miR-25 is a key SERCA2a regulating microRNA, and we showed multiple injections of antagomirs against enhance cardiac contractility function through restoration murine heart failure model. However, for clinical application, more stable suppressor would be desirable. Tough Decoy (TuD) inhibitors emerging as highly effective...

10.1016/j.ymthe.2017.11.014 article EN cc-by-nc-nd Molecular Therapy 2017-11-26

Background— Stem cell factor (SCF), a ligand of the c-kit receptor, is critical cytokine, which contributes to migration, proliferation, and survival. It has been shown that SCF expression increases after myocardial infarction (MI) may be involved in cardiac repair. The aim this study was determine whether gene transfer membrane-bound human improves function large animal model MI. Methods Results— A transmural MI created by implanting an embolic coil left anterior descending artery Yorkshire...

10.1161/circheartfailure.114.001711 article EN Circulation Heart Failure 2014-10-24

Despite a clear association between left ventricular (LV) mechanical dysfunction in end-stage heart failure and the incidence of arrhythmias, majority sudden cardiac deaths occur at earlier stages disease development. The mechanisms by which structural, mechanical, molecular alterations predispose to arrhythmias tissue level before onset LV remain unclear. In rat model pressure overload hypertrophy (PoH) produced ascending aortic banding, we correlated structural changes measured vivo with...

10.1096/fj.09-136622 article EN The FASEB Journal 2009-10-13

Abstract Extracellular vesicles (EVs) have recently emerged as an important carrier for various genetic materials including microRNAs (miRs). Growing evidences suggested that several miRs transported by EVs were particularly involved in modulating cardiac function. However, it has remained unclear what are enriched and play role the pathological condition. Therefore, we established miR expression profiles from murine normal failing hearts consecutively identified substantially altered miRs....

10.1111/jcmm.15251 article EN cc-by Journal of Cellular and Molecular Medicine 2020-06-02
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