Portraying the effect of source influx on interdependent calcium and inositol 1,4,5−trisphosphate dynamics in cardiac myocyte

Nisha Singh, Neeru Adlakha

Abstract


Calcium governs the most versatile and universal signaling mechanism in living systems which includes contraction of the cardiac tissues, information processing in the brain, release of digestive enzymes by the liver etc. High blood calcium leads to various diseases and problems like chronic fatigue and tiredness, poor memory, atherosclerosis, muscle aches and cramps, bone pain, poor sex drive, osteoporosis and broken bones, kidney stones and heart rhythm problems such as atrial fibrillation. Various investigators have been made on study of calcium signaling in cardiac myocyte to understand its mechanisms. But most of existing investigators have mainly focused on study of calcium signaling in cardiac myocyte without paying attention on interdependence of calcium signaling and inositol−1; 4; 5 trisphosphate (IP3) signaling. In the present work, we have studied a mathematical model to understand the impact of source influx of calcium and maximum rate of production of IP3 on these coupled signaling processes. This study suggests that maximum rate of production of IP3 plays a more significant role in these coupled dynamics. Also, calcium and IP3 shows a beautiful coordination with each other, which explains the role of IP3 in calcium signaling in cardiac myocyte. Such studies will provide the better understanding of various factors involved in calcium signaling in cardiac myocyte, which as a result will be of great use to biomedical scientists for making protocols for various heart diseases.

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Published: 2019-10-08

How to Cite this Article:

Nisha Singh, Neeru Adlakha, Portraying the effect of source influx on interdependent calcium and inositol 1,4,5−trisphosphate dynamics in cardiac myocyte, Commun. Math. Biol. Neurosci., 2019 (2019), Article ID 26

Copyright © 2019 Nisha Singh, Neeru Adlakha. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Commun. Math. Biol. Neurosci.

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