Ju Chen

ORCID: 0000-0001-7674-4776
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Cardiomyopathy and Myosin Studies
  • Congenital heart defects research
  • Structural Load-Bearing Analysis
  • Muscle Physiology and Disorders
  • Structural Behavior of Reinforced Concrete
  • Cardiovascular Effects of Exercise
  • Cardiac electrophysiology and arrhythmias
  • Fire effects on concrete materials
  • Ion channel regulation and function
  • RNA Research and Splicing
  • Cellular Mechanics and Interactions
  • Signaling Pathways in Disease
  • Cell Adhesion Molecules Research
  • Receptor Mechanisms and Signaling
  • RNA modifications and cancer
  • Viral Infections and Immunology Research
  • Nuclear Structure and Function
  • Cardiac Fibrosis and Remodeling
  • Mitochondrial Function and Pathology
  • RNA and protein synthesis mechanisms
  • Adipose Tissue and Metabolism
  • Concrete Corrosion and Durability
  • Autophagy in Disease and Therapy
  • Tissue Engineering and Regenerative Medicine
  • Nitric Oxide and Endothelin Effects

University of California, San Diego
2016-2025

Zhejiang University
2013-2024

Xi'an University of Technology
2024

Institute of Quality Standards and Testing Technology for Agro Products
2024

Beijing Institute of Technology
2017-2024

Chinese Academy of Agricultural Sciences
2024

Guangdong Pharmaceutical University
2024

Huazhong University of Science and Technology
2023

Peking University
2013-2023

Qinghai University
2023

Abstract —Cardiac arrhythmia is a common and often lethal manifestation of many forms heart disease. Gap junction remodeling has been postulated to contribute the increased propensity for arrhythmogenesis in diseased myocardium, although causative role vivo remains speculative. By generating mice with cardiac-restricted knockout connexin43 (Cx43), we have circumvented perinatal developmental defect associated germline inactivation this gap channel gene uncovered an essential Cx43 maintenance...

10.1161/01.res.88.3.333 article EN Circulation Research 2001-02-16

The embryonic heart and vessels are dynamic form remodel while functional. Much has been learned about the genetic mechanisms underlying development of cardiovascular system, but we just beginning to understand how changes in vessel structure influenced by hemodynamic forces such as shear stress. Recent work shown that remodeling mouse yolk sac is secondarily effected when cardiac function reduced or absent. These findings indicate proper circulation required for remodeling, have not defined...

10.1242/dev.02883 article EN Development 2007-08-24

Ca2+/calmodulin-dependent kinase II (CaMKII) has been implicated in cardiac hypertrophy and heart failure. We generated mice which the predominant isoform, CaMKIIdelta, was genetically deleted (KO mice), found that these showed no gross baseline changes ventricular structure or function. In WT KO mice, transverse aortic constriction (TAC) induced comparable increases relative weight, cell size, HDAC5 phosphorylation, hypertrophic gene expression. Strikingly, while preserved after 6-week TAC,...

10.1172/jci38022 article EN Journal of Clinical Investigation 2009-04-16

This paper presents the mechanical properties of high strength structural steel and mild at elevated temperatures. Mechanical temperatures are important for fire resistant design structures. However, current standards resistance structures mainly based on investigation hot-rolled carbon with normal strength, such as steel. The performance is unknown. Hence, an experimental program has been carried out to investigate both BISPLATE 80 (approximately equivalent ASTM A 514, EN 10137-2 Grade...

10.1061/(asce)0733-9445(2006)132:12(1948) article EN Journal of Structural Engineering 2006-11-16

The molecular basis for the focal nature of atherosclerotic lesions is poorly understood. Here, we explored whether disturbed flow patterns activate an innate immune response to form NLRP3 inflammasome scaffold in vascular endothelial cells via sterol regulatory element binding protein 2 (SREBP2). Oscillatory activates SREBP2 and induces cells. underlying mechanisms involve transactivating NADPH oxidase NLRP3. Consistently, SREBP2, 2, levels were elevated atheroprone areas mouse aortas,...

10.1161/circulationaha.113.002714 article EN Circulation 2013-07-10

Cardiac hypertrophy, initially an adaptive response of the myocardium to stress, can progress heart failure. The epigenetic signature underlying this phenomenon is poorly understood. Here, we report on genome-wide distribution seven histone modifications in adult mouse cardiomyocytes subjected a prohypertrophy stimulus vivo. We found set promoters with pattern that distinguishes specific functional classes genes regulated hypertrophy and identified 9,207 candidate active enhancers whose...

10.1073/pnas.1315155110 article EN Proceedings of the National Academy of Sciences 2013-11-27

Rationale: To date, there has been no specific marker of the first heart field to facilitate understanding contributions cardiac lineages. Cardiac arrhythmia is a leading cause death, often resulting from abnormalities in conduction system (CCS). Understanding origins and identifying markers CCS lineages are essential steps toward modeling diseases for development biological pacemakers. Objective: investigate HCN4 as precursors distinct components CCS, gain insight into second CCS. Methods...

10.1161/circresaha.113.301588 article EN Circulation Research 2013-06-07

Calcium-dependent release of vasoactive gliotransmitters is widely assumed to trigger vasodilation associated with rapid increases in neuronal activity. Inconsistent this hypothesis, intact stimulus-induced was observed inositol 1,4,5-triphosphate (IP3) type-2 receptor (R2) knock-out (KO) mice, which the primary mechanism astrocytic calcium increase-the from intracellular stores following activation an IP3-dependent pathway-is lacking. Further, our results wild-type (WT) mice indicate that...

10.1523/jneurosci.3285-12.2013 article EN cc-by-nc-sa Journal of Neuroscience 2013-05-08
Coming Soon ...