Epigenetics of Heart Failure, An issue of Heart Failure Clinics
Book Details
Format
Hardback or Cased Book
Book Series
The Clinics: Internal Medicine
ISBN-10
0443294607
ISBN-13
9780443294600
Publisher
Elsevier Health Sciences
Imprint
Churchill Livingstone
Country of Manufacture
GB
Country of Publication
GB
Publication Date
Nov 28th, 2025
Print length
240 Pages
Weight
470 grams
Product Classification:
Cardiovascular medicine
Ksh 12,950.00
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In this issue of Heart Failure Clinics, guest editor Dr. Ragavendra R. Baliga brings his considerable expertise to the topic of Epigenetics of Heart Failure. Top experts in the field explore how chemical modifications to DNA and histones influence gene expression without altering the genetic code, contributing to the development and progression of heart failure. Factors such as DNA methylation, histone modifications, and non-coding RNAs can regulate key pathways involved in cardiac remodeling, inflammation, and fibrosis. Environmental influences like diet, stress, and toxins can also impact these epigenetic changes, potentially worsening heart function. Understanding these mechanisms may lead to novel therapeutic targets for preventing or treating heart failure at the molecular level.
- Contains 18 relevant, practice-oriented topics including DNA damage response in hereditary cardiomyopathies; novel insights from mammals of extreme longevity into genetic and epigenetic regulation of heart regeneration and repair; epigenetic control in clonal hematopoiesis and impact on heart failure; pharmacological and lifestyle interventions to modulate the epigenome in heart failure; epigenetics in dilated cardiomyopathy; and more
- Provides in-depth clinical reviews on epigenetics of heart failure, offering actionable insights for clinical practice
- Presents the latest information on this timely, focused topic under the leadership of experienced editors in the field. Authors synthesize and distill the latest research and practice guidelines to create clinically significant, topic-based reviews
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