Effects of d-galactose-induced ageing on the heart and its potential interventions

J Cell Mol Med. 2018 Mar;22(3):1392-1410. doi: 10.1111/jcmm.13472. Epub 2018 Jan 24.

Abstract

Ageing is a strong independent risk factor for disability, morbidity and mortality. Post-mitotic cells including those in the heart are a particular risk to age-related deterioration. As the occurrence of heart disease is increasing rapidly with an ageing population, knowledge regarding the mechanisms of age-related cardiac susceptibility and possible therapeutic interventions needs to be acquired to prevent advancing levels of heart disease. To understand more about the ageing heart, numerous aged animal models are being used to explore the underlying mechanisms. Due to time-consuming for investigations involving naturally aged animals, mimetic ageing models are being utilized to assess the related effects of ageing on disease occurrence. d-galactose is one of the substances used to instigate ageing in various models, and techniques involving this have been widely used since 1991. However, the mechanism through which d-galactose induces ageing in the heart remains unclear. The aim of this review was to comprehensively summarize the current findings from in vitro and in vivo studies on the effects of d-galactose-induced ageing on the heart, and possible therapeutic interventions against ageing heart models. From this review, we hope to provide invaluable information for future studies and based on the findings from experiments involving animals, we can inform possible therapeutic strategies for the prevention of age-related heart diseases in clinical settings.

Keywords: ageing; d-galactose; heart; mitochondria.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Aging / drug effects*
  • Aging / genetics
  • Aging / metabolism
  • Aging / pathology
  • Animals
  • Antioxidants / pharmacology
  • Apoptosis / drug effects
  • Apoptosis / genetics
  • Calcium / metabolism*
  • Cardiotonic Agents / pharmacology
  • Galactose / administration & dosage*
  • Gene Expression Regulation
  • Glycation End Products, Advanced / agonists
  • Glycation End Products, Advanced / genetics*
  • Glycation End Products, Advanced / metabolism
  • Heart / drug effects*
  • Heart / physiopathology
  • Humans
  • Mice
  • Mitochondria, Heart / drug effects
  • Mitochondria, Heart / metabolism
  • Mitochondria, Heart / pathology
  • Models, Animal
  • Myocytes, Cardiac / drug effects*
  • Myocytes, Cardiac / metabolism
  • Myocytes, Cardiac / pathology
  • Oxidative Stress
  • Rats
  • Reactive Oxygen Species / agonists
  • Reactive Oxygen Species / antagonists & inhibitors
  • Reactive Oxygen Species / metabolism
  • Tumor Suppressor Protein p53 / agonists
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism
  • beta-Galactosidase / genetics
  • beta-Galactosidase / metabolism

Substances

  • Antioxidants
  • Cardiotonic Agents
  • Glycation End Products, Advanced
  • Reactive Oxygen Species
  • Tumor Suppressor Protein p53
  • beta-Galactosidase
  • Calcium
  • Galactose