(All fields required)
Please enter a valid email.
Please enter your name.
No Photo information has been entered yet.
To begin editing, right-click and select "Edit".
birth, cardiac muscle cells stop proliferating and the heart grows primarily by
increasing the size of cells. In this
publication, Sengupta et al report a
novel genetic regulatory mechanism whereby FoxO and FoxM1 transcription factors
regulate the withdrawal of cardiac muscle cells from cell cycle. An additional novel finding is that these transcription factors are
sensitive to the metabolic state of heart muscle that undergoes a switch from
using primarily glucose to using fatty acids for energy during the neonatal
Together these studies define a completely new regulatory mechanism for control of
neonatal cardiomyocyte cell withdrawal. Since these same regulatory mechanisms are
associated with adult cardiac disease, these studies also have potential
implications for cardiac repair and regeneration as well as development of new
Cardiovascular diseases ultimately result in the
failure of the heart to achieve its pumping function. This review discusses the
development of new drugs that aim at maintaining the heart’s function with
cardiovascular disease. This can primarily be achieved through the modulation
of the neuro-hormonal cardiac response. Neuro-hormonal signals activate G
protein coupled receptors which initiate cardio-protective and deleterious
While the currently available G protein coupled
receptors drugs (i.e. beta-blockers or Angiotensin Receptors Blockers)
indistinctly target all the G protein coupled receptors intracellular pathways,
the development of biased G protein coupled receptor ligands constitutes a
ground-breaking approach for the treatment of cardiovascular diseases because
they specifically activate cardio-protective signaling pathways. Additionally,
drugs that would acutely restore contractility (i.e. PKCa or Calcium Calmodulin Kinase II inhibitors)
could constitute a significant adjunct to the currently available treatment
Furthermore, a potential interesting therapeutic approach would be to
reduce the levels of a non-contractile intracellular calcium pool known to
contribute to the development of cardiac hypertrophy (i.e. non-selective cationic
TRPC channels inhibitors). As the heart failure epidemic continues to rise
despite the available treatments, the development of new drugs targeting all
stages of heart disease is vital.
3333 Burnet Avenue, Cincinnati, Ohio 45229-3026 | 1-513-636-4200 | 1-800-344-2462 | TTY: 1-513-636-4900
New to Cincinnati Children’s or live outside of the Tristate area? 1-877-881-8479
© 1999-2014 Cincinnati Children's Hospital Medical Center