Gregory R. Bock & Jamie A. Goode 
Heart Failure [PDF ebook] 
Molecules, Mechanisms and Therapeutic Targets

Heart failure is the main cause of death and disability in the
industrialized world. There is a major need for novel therapeutics
for prevention and reversal of cardiac pathology associated with
heart failure and cardiac enlargement. Over recent years, dramatic
progress has been made in unravelling the cellular circuitry
involved in cardiac failure, as well as in normal cardiac growth,
development and apoptosis. This work has revealed new and
unexpected therapeutic targets in the heart. In addition, advances
in understanding the role of stem cells in cardiac physiology have
suggested strategies for cardiac repair and regeneration once
thought impossible.

This book describes the work of leading investigators studying
the basic mechanisms of cardiac growth, function and dysfunction.
There are also exciting contributions from researchers developing
novel therapeutic strategies for cardiac disease. The unique
feature is the discussions amongst the contributors, which always
return to the same basic problem: how can new data from biological
studies be used to design novel therapies for the treatment of
cardiac dysfunction following myocardial infarction, hypertension
and other disorders?

With its strong emphasis on translational research, this book
will appeal to both scientists and clinicians interested in
diminishing the impact of the current epidemic of cardiac
diseases.

Tabela de Conteúdo

Introduction (Eric N. Olson).

Control of cardiac hypertrophy and heart failure by histone
acetylation/deacetylation (Eric N. Olson, Johannes Backs and
Timothy A. Mc Kinsey) .

Discussion.

A novel mechanism of mechanical stress-induced hypertrophy
(Hiroshi Akazawa, Yunzeng Zou and Issei Komuro) .

Discussion.

Controlling cardiomyocyte survival (N. de Jonge, M. J.
Goumans, Daan Lips, Rutger Hassink, Eva J. Vlug, Roy van der Meel,
Christopher Donald Emmerson, Joppe Nijman, Leon de Windt and Pieter
A. Doevendans) .

Discussion.

Mechanisms of angiotensin II-dependent progression to heart
failure (Mona Nemer, Nassim Dali-Youcef, Hao Wang, Anne Aries
and Pierre Paradis) .

Discussion.

Alterations in myocardial gene expression as a basis for
cardiomyopathies and heart failure (Matthew R. Taylor and
Michael R. Bristow) .

Discussion.

Role of the insulin-like growth factor 1
(IGF1)/phosphoinositide-3-kinase (PI3K) pathway mediating
physiological cardiac hypertrophy (Julie R. Mc Mullen and Seigo
Izumo).

Discussion.

Role of Akt in cardiac growth and metabolism(Anthony J.
Muslin and Brian De Bosch).

Discussion.

Novel therapy for heart failure and exercise-induced ventricular
tachycardia based on ‘fixing’ the leak in ryanodine
receptors (Andrew R. Marks).

Discussion.

General discussion I.

Phospholamban as a therapeutic modality in heart failure
(Guoxiang Chu and Evangelia G. Kranias).

Discussion.

Sarcomere protein gene mutations and inherited heart disease: a
b-cardiac myosin heavy chain mutation causing endocardial
fibroelastosis and heart failure (Mitsuhiro Kamisago, Joachim P.
Schmitt, Dennis Mc Namara, Christine Seidman and Jonathan G.
Seidman).

Discussion.

The cardiomyocyte cell cycle (Pascal J. E. Lafontant and
Loren J. Field).

Discussion.

Restoration of cardiac function with progenitor cells (Carmen
Urbich, Lothar Rössig and Stefanie Dimmeler).

Discussion.

Signalling pathways in cardiac regeneration (Maria Paola
Santini, Nadine Winn and Nadia Rosenthal).

Discussion.

Beyond small molecule drugs for heart failure: prospects for
gene therapy (Kenneth R. Chien).

Discussion.

Dual roles of telomerase in cardiac protection and repair
(Michael D. Schneider).

Discussion.

Final general discussion.

Closing remarks: historical perspective (Arnold M.
Katz).

Index of contributors.

Subject index.

Sobre o autor

The Novartis Foundation is an international scientific and educational charity which promotes the study and general knowledge of science and in particular encourages international co-operation in scientific research.