The Molecular Biology of Chronic Heart Failure

The Molecular Biology of Chronic Heart Failure

Dhavendra Kumar
ISBN: 9781615045563 | PDF ISBN: 9781615045570
Copyright © 2013 | 90 Pages | Publication Date: 02/01/2013

BEFORE YOU ORDER: You may have Academic or Corporate access to this title. Click here to find out: 10.4199/C00071ED1V01Y201212GMM003

Ordering Options: Paperback $30.00   E-book $24.00   Paperback & E-book Combo $37.50

Why pay full price? Members receive 15% off all orders.
Learn More Here

Read Our Digital Content License Agreement (pop-up)

Purchasing Options:


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).

Table of Contents



About the Author(s)

Dhavendra Kumar, Institute of Molecular and Experimental Medicine, Cardiff University School of Medicine, University Hospital of Wales, UK

Reviews
Browse by Subject
ACM Books
IOP Concise Physics
0 items
LATEST NEWS

Newsletter
Note: Registered customers go to: Your Account to subscribe.

E-Mail Address:

Your Name: