Exploring Phosphatase and Tensin Homologue Deleted on Chromosome Ten (PTEN) as a Potential Therapeutic Target for Cardiac Hypertrophy

Abstract

While cardiovascular diseases continue to be the foremost cause of death worldwide, heart failure constitutes a major segment responsible for these mortalities. Heart failure results from exhausted cardiac myocytes that lose the ability to pump blood effectively. Cardiac hypertrophy is a condition of the heart wherein the thickening of the cardiomyocytes leads to an abnormal enlargement of the myocardium. The PI3K/AKT/mTOR signaling pathway plays a pivotal role in the development of cardiac hypertrophy by regulating cell growth, proliferation, metabolism, and survival in cardiac myocytes. The phosphatase and tensin homologue deleted on chromosome ten (PTEN) is a membrane-bound lipid phosphatase that facilitates dephosphorylation of PIP3 to PIP2, thus preventing the hyperactivation of the PI3K/AKT/mTOR signaling pathway. Augmentation of PTEN expression and activity can hinder cardiac hypertrophy and mitigate the risk of heart failure. The present review discusses the role of PTEN in controlling unchecked cardiomyocyte proliferation and provides an account of the novel findings from current research on the noncoding RNAs and proteins interacting with PTEN. The review further discusses the pharmacological agents that restore PTEN expression and function and may emerge as effective therapeutics for the treatment of cardiac hypertrophy.