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Pathophysiology of Cardiac Performance

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Typical heart performance is influenced by heart rate, rhythm, myocardial contraction, and metabolism or blood flow. The cardiac muscle exhibits distinct electrophysiological features, including pacemaker activity and calcium channel control, which play a vital role in the heart's response to various drugs. The autonomic nervous system, comprising the sympathetic and parasympathetic branches, regulates heart rate. Sympathetic activation increases heart rate, while parasympathetic activation...

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Related Experiment Video

Updated: Nov 22, 2025

High Efficiency Differentiation of Human Pluripotent Stem Cells to Cardiomyocytes and Characterization by Flow Cytometry

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Published on: September 23, 2014

Yulink, predicted from evolutionary analysis, is involved in cardiac function.

Ming-Wei Kuo¹, Hsiu-Hui Tsai¹, Sheng-Hung Wang¹

¹Institute of Stem Cell and Translational Cancer Research, Chang Gung Memorial Hospital at Linkou, Taoyuan, 333, Taiwan.

Journal of Biomedical Science

|January 11, 2021

Summary

Yulink is a conserved gene crucial for cardiomyocyte function. Its deficiency disrupts calcium cycling via Serca2 regulation, potentially causing heart rhythm disorders in humans and zebrafish.

Keywords:

Ca2+ cycling Cardiomyocytes PPARγ SERCA2 Yulink

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Area of Science:

Cardiovascular Biology
Genomics
Molecular Mechanisms

Background:

Yulink is an evolutionarily conserved gene identified through comparative genomics.
Its function in cardiomyocytes remains largely unknown.
This study investigates Yulink's role in cardiomyocyte function and its regulatory pathways.

Purpose of the Study:

To determine the involvement of Yulink in cardiomyocyte functions.
To elucidate the molecular mechanisms underlying Yulink's regulation.
To assess Yulink's conservation and function across species.

Main Methods:

Gene knockdown using morpholino and shRNA in zebrafish, mouse HL-1, and human iPSC-derived cardiomyocytes.
Quantification of mRNA and protein expression via qPCR and Western blot.
Functional assays including Ca2+ imaging, DNA binding, and agonist treatments.

Main Results:

Yulink knockdown in zebrafish caused cardiac dysfunction.
In cardiomyocytes, Yulink deficiency disrupted Ca2+ cycling and reduced SERCA2 expression, mediated by PPARγ.
Overexpression of Yulink, PPARγ, or SERCA2 rescued Yulink knockdown phenotypes.

Conclusions:

Yulink is essential for maintaining normal Ca2+ cycling in cardiomyocytes.
Yulink regulates SERCA2 expression, likely through PPARγ.
Yulink deficiency may contribute to cardiac arrhythmias due to impaired Ca2+ handling.