Aizhu Lu
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View article: Association between C-reactive protein-triglyceride-glucose index and the risk of cardiovascular-kidney metabolic syndrome progression:The Kailuan Study
Association between C-reactive protein-triglyceride-glucose index and the risk of cardiovascular-kidney metabolic syndrome progression:The Kailuan Study Open
Background The American Heart Association (AHA) has proposed the concept of cardiovascular-kidney-metabolic (CKM) syndrome to describe the interrelationships between heart, kidney, and metabolic diseases. Advanced cardiovascular-kidney-met…
View article: Wnt/β-catenin signaling regulates cardiac Cx43 in a metabolic substrate-dependent manner
Wnt/β-catenin signaling regulates cardiac Cx43 in a metabolic substrate-dependent manner Open
View article: Wnt/β-catenin Signaling Regulates Cardiac Cx43 in a Metabolic Substrate-Dependent Manner
Wnt/β-catenin Signaling Regulates Cardiac Cx43 in a Metabolic Substrate-Dependent Manner Open
View article: High Glucose Sensitizes Male and Female Rat Cardiomyocytes to Wnt/β-Catenin Signaling
High Glucose Sensitizes Male and Female Rat Cardiomyocytes to Wnt/β-Catenin Signaling Open
Wnt/β-catenin signaling has been shown to regulate gene expressions in cardiomyocytes. However, it is not known if this effect is dependent on the sex of cells or the glucose level in the culture medium. In the present study, ventricular m…
View article: Inhibition of Wnt/β‐catenin signaling upregulates Na<sub>v</sub>1.5 channels in Brugada syndrome <scp>iPSC</scp>‐derived cardiomyocytes
Inhibition of Wnt/β‐catenin signaling upregulates Na<sub>v</sub>1.5 channels in Brugada syndrome <span>iPSC</span>‐derived cardiomyocytes Open
The voltage‐gated Na v 1.5 channels mediate the fast Na + current ( I Na ) in cardiomyocytes initiating action potentials and cardiac contraction. Downregulation of I Na , as occurs in Brugada syndrome (BrS), causes ventricular arrhythmias…
View article: Wnt/β-Catenin Signaling Causes Sinoatrial Node Dysfunction by Inhibition of T-type Calcium Current
Wnt/β-Catenin Signaling Causes Sinoatrial Node Dysfunction by Inhibition of T-type Calcium Current Open
View article: Inhibition of β-catenin Protects Mouse Hearts From Ventricular Arrhythmias After Myocardial Infarction Independent of Ion Channel Gene Changes
Inhibition of β-catenin Protects Mouse Hearts From Ventricular Arrhythmias After Myocardial Infarction Independent of Ion Channel Gene Changes Open
Wnt/β-catenin signaling is activated in the heart after myocardial infarction (MI). This study aims to investigate if β-catenin deletion affects post-MI ion channel gene alterations and ventricular tachycardias (VT). MI was induced by perm…
View article: Cardiomyocyte-specific deletion of β-catenin protects mouse hearts from ventricular arrhythmias after myocardial infarction
Cardiomyocyte-specific deletion of β-catenin protects mouse hearts from ventricular arrhythmias after myocardial infarction Open
View article: Inhibition of β-catenin Protects Mouse Hearts From Ventricular Arrhythmias After Myocardial Infarction Independent of Ion Channel Gene Changes
Inhibition of β-catenin Protects Mouse Hearts From Ventricular Arrhythmias After Myocardial Infarction Independent of Ion Channel Gene Changes Open
The Wnt/β-catenin signaling regulates ion channel gene expressions in cardiomyocytes. Because Wnt/β-catenin signaling is activated in myocardial infarction (MI), this study aims to investigate if β-catenin inhibition affects post-MI ion ch…
View article: Inhibition of β-catenin Increases Voltage-gated Na <sup>+</sup> Current in Brugada Syndrome Cardiomyocytes
Inhibition of β-catenin Increases Voltage-gated Na <sup>+</sup> Current in Brugada Syndrome Cardiomyocytes Open
View article: GATA6 is a regulator of sinus node development and heart rhythm
GATA6 is a regulator of sinus node development and heart rhythm Open
Significance GATA6 is a key regulator of sinus node (SAN) development. Loss of one Gata6 allele disrupts patterning and size of the SAN. GATA6 plays cell autonomous as well as non-cell autonomous functions in several cell types required fo…
View article: <i>De Novo</i> Human Cardiac Myocytes for Medical Research: Promises and Challenges
<i>De Novo</i> Human Cardiac Myocytes for Medical Research: Promises and Challenges Open
The advent of cellular reprogramming technology has revolutionized biomedical research. De novo human cardiac myocytes can now be obtained from direct reprogramming of somatic cells (such as fibroblasts), from induced pluripotent stem cell…