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Dysfunctional survival-signaling and stress-intolerance in aged murine and human myocardium

Authors
  • Peart, Jason N.
  • Pepe, Salvatore
  • Reichelt, Melissa E.
  • Beckett, Nikkie
  • See Hoe, Louise
  • Ozberk, Victoria
  • Niesman, Ingrid R.
  • Patel, Hemal H.
  • Headrick, John P.1, 2, 3, 4, 5, 6, 7, 8, 7, 9, 10, 11
  • 1 Heart Foundation Research Centre
  • 2 Griffith Health Institute
  • 3 Griffith University
  • 4 Heart Research
  • 5 Murdoch Children's Research Institute
  • 6 Department of Paediatrics
  • 7 University of Melbourne
  • 8 Department of Physiology
  • 9 VA San Diego Healthcare System
  • 10 Department of Anesthesiology
  • 11 University of California San Diego
Type
Published Article
Journal
Experimental Gerontology
Publication Date
Jan 01, 2013
Accepted Date
Nov 26, 2013
Volume
50
Pages
72–81
Identifiers
DOI: 10.1016/j.exger.2013.11.015
Source
Elsevier
Keywords
License
Unknown

Abstract

•Aging repressed ischemic tolerance in human atrial tissue and mouse hearts.•Aging reduced cardioprotection via preconditioning (hormesis) and GPCR/PKC activation.•Protection via modulation of key mitochondrial effectors of protection was preserved.•Survival signal transduction from receptors to mitochondria is dysfunctional, in association with membrane/caveolar changes.•Protein expression in aged mouse heart further favors mitochondrial injury/cell death.

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