MiRNA Deregulation in Cardiac Aging and Associated Disorders

Robin Verjans, Marc van Bilsen, Blanche Schroen*

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapterAcademic

Abstract

The prevalence of age-related diseases is increasing dramatically, among which cardiac disease represents the leading cause of death. Aging of the heart is characterized by various molecular and cellular hallmarks impairing both cardiomyocytes and noncardiomyocytes, and resulting in functional deteriorations of the cardiac system. The aging process includes desensitization of beta-adrenergic receptor (beta AR)-signaling and decreased calcium handling, altered growth signaling and cardiac hypertrophy, mitochondrial dysfunction and impaired autophagy, increased programmed cell death, lowgrade inflammation of noncanonical inflammatory cells, and increased ECM deposition.

MiRNAs play a fundamental role in regulating the processes underlying these detrimental changes in the cardiac system, indicating that MiRNAs are crucially involved in aging. Among others, MiR-34, MiR-146a, and members of the MiR-17-92 cluster, are deregulated during senescence and drive cardiac aging processes. It is therefore suggested that MiRNAs form possible therapeutic targets to stabilize the aged failing myocardium.

Original languageEnglish
Title of host publicationInternational Review of Cell and Molecular Biology
Subtitle of host publicationMiRNAs in Aging and Cancer
EditorsLorenzo Galluzzi, Ilio Vitale
PublisherElsevier Science
Chapter5
Pages207-263
Number of pages57
Volume334
ISBN (Print)978-0-12-811868-9
DOIs
Publication statusPublished - 2017

Publication series

SeriesInternational Review of Cell and Molecular Biology
Volume334
ISSN1937-6448

Keywords

  • ACUTE MYOCARDIAL-INFARCTION
  • PRESERVED EJECTION FRACTION
  • DIASTOLIC HEART-FAILURE
  • KAPPA-B ACTIVATION
  • GROWTH-FACTOR-BETA
  • CARDIOVASCULAR-DISEASE ENTERPRISES
  • SARCOPLASMIC-RETICULUM CA2+-ATPASE
  • INDUCED CARDIOMYOCYTE HYPERTROPHY
  • HYPOXIA-INDUCIBLE FACTOR-1-ALPHA
  • REGULATES GLUCOSE-METABOLISM

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