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The Molecular Biology of Chronic Heart Failure (Paperback)
Loot Price: R1,153
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The Molecular Biology of Chronic Heart Failure (Paperback)
Series: Colloquium Series on Genomic and Molecular Medicine
Expected to ship within 10 - 15 working days
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The clinical syndrome of chronic heart failure (CHF) is the
hallmark of progressive cardiac decompensation, one of the most
common chronic medical conditions that affect around 2% of the
adult population worldwide irrespective of ethnic and geographic
origin (Anonymous). Apart from ischemic heart disease,
hypertension, infection, and inflammation, several other etiologic
factors account for irreparable and irreversible myocardial damage
leading to heart failure (HF). Genetic and genomic factors are now
increasingly identified as one of the leading underlying factors
(Arab and Liu 2005). These factors may be related to pathogenic
alterations (mutation or polymorphism) within specific cardiac
genes, mutations in genes incorporating single or multiple
molecular pathways (protein families) relevant to cardiac structure
and/or function, genetic or genomic polymorphisms of uncertain
significance (gene variants, single-nucleotide polymorphisms
(SNPs), and copy number variations (CNVs)), and epigenetic or
epigenomic changes that influence cardiac gene functions scattered
across the human genome. Recent genetic and genomic studies in both
systolic and diastolic ventricular dysfunction, the hallmark of
CHF, have revealed a number of mutations in genes belonging to
specific cardiac protein families. For example, around 200
mutations are now known to exist in around 15 genes coding for
several different types of sarcomere proteins (Liew and Dzau 2004).
The sarcomere protein family, alone, accounts for the bulk of
inherited cardiomyopathies including hypertrophic cardiomyopathy
(HCM), dilated cardiomyopathy (DCM), restrictive cardiomyopathy
(RCM), and left ventricular (LV) non-compaction (LVNC). In
addition, there are several other potentially relevant factors
involving different genes and genome-level elements. This article
presents a systematic account on the available factual information
and interpretations based on genetic and genomic studies in CHF
(Liew and Dzau 2004). Genomic and molecular approaches have opened
the way for a renewed debate for taxonomy of CHF (Ashrafian and
Watkins 2007). The review draws attention to the potential
diagnostic and therapeutic implications of genomic and
transcriptional profiling in HF and translational genomics research
that is likely to permit greater personalization of prevention and
treatment strategies to address the complexities of managing
clinical HF (Creemers, Wilde et al. 2011).
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