Preface - Ous-research.no

Molecular Cardiology
Leader:
Håvard Attramadal Professor, MD, PhD (OUH/UiO)
Scientific staff:
M. Shakil Ahmed, Senior Scientist, PhD (OUH)
Vladimir N. Martinov, PhD, Postdoc (NRC)
Thomas G. von Lueder, MD, Postdoc, (OUH)
Jørgen A. Gravning, MD, PhD-student (OUH)
Ingvild Tronstad Moe, MD, PhD-Student (NCCD/UiO)
Tuyet Anh Pham, MD, PhD-student (SENRHA)
Eva Maria Rehbinder, MD, PhD-student (NCCD)
Fermí Montó Guillot, MSc, PhD-student/Exchange scientist
(Valencia University School of Pharmacy)
Else Marie Valbjørn Hagelin, MSc, Senior Engineer (SENRHA)
Professor Håvard Attramadal
Research Area
Heart failure, the common end-point in cardiac disease of
diverse etiologies, is a major cause of morbidity and mortality
in affluent societies. Indeed, the incidence and prevalence
of heart failure in these countries are increasing due
to altered demographics with increased proportion of the
elderly, as well as increased survival of myocardial infarction.
Despite implementation of several new treatment modalities
during the last 20 years, heart failure is still a progressive
and ominous disease indicating that important pathogenic
mechanisms remain unmodified by the most current treatment
modalities.
In evolving heart failure multiple compensatory actions
are triggered in order to maintain cardiac output, among
which is activation of the sympathetic nervous system, the
renin-angiotensin system, as well as a number of autocrine/
paracrine factors synthesized in myocardial tissue. The
compensatory actions also reflect alterations in of cardiac
structure, collectively called cardiac remodeling. These
structural alterations comprise dilatation of the ventricular
chambers, myocardial hypertrophy and fibrosis. Although
cardiac remodeling may initially balance loss of contractile
force, the continuum of these structural alterations often
feeds into vicious circles leading to progression of cardiac
dysfunction and overt heart failure. Increasing evidence
points to myocardial hypertrophy, fibrosis, and dilatation of
the ventricular cavities as independent risk factors of heart
failure. Indeed, recognition of these structural alterations
of the heart is implemented in the new recommendations
for the evaluation and management of chronic heart failure
recently published by the American College of Cardiology/
American Heart Association Task Force. According to these
recommendations, which are meant to complement the
New York Heart Association (NYHA) functional classification,
patients are to be stratified according to risk factors for
developing heart failure, including the absence or presence
of structural alterations of the heart.
Despite substantial new insights into the mechanisms of
myocardial hypertrophy and fibrosis, many of the nodal
points that orchestrate these structural alterations still
remain to be identified. Furthermore, current knowledge
largely precludes from deciphering of adaptive versus maladaptive
cellular responses to insufficient cardiac output.
Thus, the focus of our research group is to unravel the signal
transduction mechanisms leading to dysfunctional signaling
responses and pathologic remodeling of the heart. The
purpose of these investigations is to provide new knowledge
of disease mechanisms enabling development of novel
pharmacological interventions for heart failure.
Our research group is a multidisciplinary team of experts
in gene technology, molecular and cellular biology, as well
as experimental and clinical medicine. The research efforts
comprise studies of isolated cardiac myocytes, integrated
physiology in transgenic animal models, as well as clinical
investigations. Our research group is member of Center for
Heart Failure Research, University of Oslo (www.heartfailure.
no), a thematic research initiative and focus area of research
selected by the Faculty of Medicine. Center for Heart Failure
Research has also become a regional research network
sponsored by Helse Sør-Øst Regional Health Authority. The
Institute for Surgical Research provides infrastructure with
state-of-the-art equipment for high-resolution echocardiography
and integrated physiologic assessment of cardiac
function in transgenic mice.
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