Eun-Hwa Jang
Seoul National University · 医学
研究室紹介
Professor Eun-Hwa Jang's research lab focuses on the molecular and cellular mechanisms underlying cardiac dysfunction in heart failure and cancer, with a particular emphasis on nitric oxide signaling, calcium homeostasis, and metabolic remodeling in the heart. The lab investigates the role of neuronal nitric oxide synthase (nNOS) and transglutaminase 2 (TG2) in regulating cardiac contractility and oxidative stress, especially under pathological conditions such as hypertension and heart failure. Additionally, the lab explores metabolic reprogramming in cardiomyocytes and its impact on energy metabolism and function, as well as the therapeutic potential of targeted agents in gastric cancer. These studies integrate molecular biology, cardiac physiology, and nuclear imaging to uncover novel mechanisms and therapeutic strategies.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15Neuronal nitric oxide synthase (nNOS or NOS1) is the major endogenous source of myocardial nitric oxide (NO), which facilitates cardiac relaxation and modulates contraction. In the healthy heart it regulates intracellular Ca(2+), signalling pathways and oxidative homeostasis and is upregulated from early phases upon pathogenic insult. nNOS plays pivotal roles in protecting the myocardium from increased oxidative stress, systolic/diastolic dysfunction, adverse structural remodelling and arrhythmi
Neuronal nitric oxide synthase (NOS1 or nNOS) exerts negative inotropic and positive lusitropic effects through Ca(2+) handling processes in cardiac myocytes from healthy hearts. However, underlying mechanisms of NOS1 in diseased hearts remain unclear. The present study aims to investigate this question in angiotensin II (Ang II)-induced hypertensive rat hearts (HP). Our results showed that the systolic function of left ventricle (LV) was reduced and diastolic function was unaltered (echocardiog
Lower neck LN involvement, high SUVmax in pretreatment <sup>18</sup>F-FDG PET-CT, and large tumour size were predictive factors for DM in patients of OPC.
The myocardium in hypertensive heart exhibits decreased fatty acid utilization and contractile dysfunction, leading to cardiac failure. However, the causal relationship between metabolic remodeling and cardiomyocyte contractility remains unestablished. Transglutaminase 2 (TG2) has been known to promote ATP production through the regulation of mitochondrial function. In this study, we investigated the involvement of TG2 in cardiomyocyte contraction under fatty acid supplementation. Using TG2 inhi
Heart failure and cardiac arrhythmias are the leading causes of mortality and morbidity worldwide. However, the mechanism of pathogenesis and myocardial malfunction in the diseased heart remains to be fully clarified. Recent compelling evidence demonstrates that changes in the myofilament Ca(2+) sensitivity affect intracellular Ca(2+) homeostasis and ion channel activities in cardiac myocytes, the essential mechanisms responsible for the cardiac action potential and contraction in healthy and di
This study demonstrates the antitumor activity and significant cell cycle arrest effect of ZD1839 against human gastric carcinoma cells and its synergistic interaction with LOHP and PTX. These results provide a preclinical rationale for the clinical development of ZD1839 and its use in combination with LOHP or PTX against human gastric cancers that express EGFR.