Explore chapters and articles related to this topic
Rosmarinic Acid: A Boon in the Management of Cardiovascular Disease
Published in Mahfoozur Rahman, Sarwar Beg, Mazin A. Zamzami, Hani Choudhry, Aftab Ahmad, Khalid S. Alharbi, Biomarkers as Targeted Herbal Drug Discovery, 2022
Md. Adil Shaharyar, Mahfoozur Rahman, Kumar Anand, Chowdhury Mobaswar Hossain, Imran Kazmi, Sanmoy Karmakar
Acute myocardial infarction (AMI) and arrhythmia are a menace to the society and a great cause of hospitalization and mortality respectively. The cellular calcium level is regulated by both Sarcoplasmic reticulum Ca2+ ATPase (SERCA2) and Ryanodine receptor (RyR2), respectively. The protocol was designed in such a way so as to investigate whether rosmarinic acid can safeguard cardiac functions against AMI and arrhythmia induced by Isoproterenol, modulated by both SERCA2 and RyR2 genotypically. For mechanism of rosmarinic acid in myocardial infarction refer to Figure 10.1 (Javidanpour et al., 2018).
Agrochemical-mediated cardiotoxicity in zebrafish embryos/larvae: What we do and where we go
Published in Critical Reviews in Environmental Science and Technology, 2023
Yang Yang, Yue Tao, Zixu Li, Yunhe Cui, Jinzhu Zhang, Ying Zhang
Ca2+ is essential for cardiac contraction and diastole, and imbalances in Ca2+ homeostasis in cardiomyocytes are often an important trigger of cardiac failure (Li & Hwang, 2015). Briefly, activation of voltage-dependent L-type Ca channels (DHP receptors) upon membrane depolarization causes Ca2+ enter into the cytoplasmic matrix and activate RYR2 via a Ca2+-induced Ca release mechanism, causing the release of Ca2+ from the sarcoplasmic reticulum (SR) and binding of Ca2+ to troponin C and ultimately myocardial contraction (Eisner et al., 2017). Continuous contraction of the myocardium cannot cause periodic beating of cardiac cells, and myocardial diastole occurs when the Ca2+ bound to troponin C is pumped out of the cell by the Na+/Ca2+ exchanger or pumped back into the SR by the sarco(endo)plasmic Ca2+-ATPase in the nonfunctional region of the SR (Bovo et al., 2013) (Figure 5).