G protein couple receptor kinase 2 and 5 (GRK2 and GRK5) are the main negative regulators of ? Adrenoceptor activation, which plays an important role in cardiac function and contractility. Changed GRK2 levels are associated with heart failure, and it has been highlighted that the GRK2 level is upregulated in cardiac failure patients. The increased expression and activity of GRK2 have been reported as harmful to the heart and playing an important role in the development of cardiac hypertrophy. GRK5 might also be linked to the development of cardiac hypertrophy. Several studies indicating that GRK5 plays an important role in pathological cardiac hypertrophy in a non-canonical manner. However, little is known about GRK2 and GRK5 related molecular signaling and their important role in the progression of cardiac myopathy is not well elucidated. Thus, our reserach aims to illustrates the mechanistic role of GRK2 and GRK5 in cardiac hypertrophy and identify the potential molecular mechanisms by which GRK2 and GRK5 participate in its progression. Additionally aims to assess the potential of GRK2 and GRK5 as therapeutic targets by attenuating their kinases activities in animal models of cardiac hypertrophy.  

ASMA ALONAZI, graduated from King Saud University (KSU) with bachelor’s degree in Pharmaceutical Sciences (BSc Pharm.) in 2007. Next, she earned master’s degree in Pharmacology (MSc) in 2013. Then, she promoted to a lecturer in the pharmacology and toxicology department at KSU. In 2015, ASMA joined Department of Cell Physiology and Pharmacology at University of Leicester in United Kingdom to pursue her PhD. On November 2019, ASMA award Doctor of Philosophy in Cell Physiology and Pharmacology (PhD) from University of Leicester in UK. Currently, Dr ALONAZI, working as Assistant Professor in Department of Pharmacology and Toxicology at College of Pharmacy in KSU. Her primary research field is Molecular Pharmacology of cardiovascular disease. Particularly, G protein coupled receptors (GPCRs) function, regulation, classical and non-classical signaling pathways in cardiac hypertrophy and hypertensive vascular remodeling.