Cellular and molecular biology of cardiac hypertrophy Academic Article uri icon


  • Cardiovascular system at the cellular level adapts to chronic haemodynamic changes by altering gene expression. Cardiac cell-specific expressions of many contractile protein genes are regulated at the transcriptional level by the interaction of activator proteins with specific cis-acting sequences. A number of positive and negative cis-acting elements from upstream of the basal promoter region and some of their trans-acting protein binding factors have been characterized. Recent epidemiological studies implicated left ventricular hypertrophy (LVH) as a premonitory symptom of mortality from many cardiovascular complications. Although cardiac hypertrophy by a chronic haemodynamic overload per se is not a pathological rather biological adaptive response of heart, heart failure as a final form of hypertrophy is an obvious disorder producing high mortality. Qualitative changes in the actin-myosin genomic expression such as re-expression of fetal isoforms, through the induction of immediate-early genes (proto-oncogenes), allow the hypertrophied cardiac fibre to develop a normal active tension to the sustained load at the cost of its maximal shortening velocity, thus inducing a pathological state. Multiple lines of evidence support the existence and functional integration of a variety of humoral factors within the . heart, and may participate in the genesis of LVH. The renin-angiotensin system (RAS) has been suggested to play a pivotal role in the regulation of cardiac cell growth and LVH. Other humoral mechanisms such as sympathetic nervous system and endothelin vaso-constrictors have also been implicated. Thus, the elucidation of the cellular and molecular biology of normal cardiac growth, development and hypertrophy may hopefully lead to the development of novel therapeutic strategies to cardiac failure.

published proceedings


author list (cited authors)

  • Reddy, D. S.

complete list of authors

  • Reddy, DS

publication date

  • January 1997