Current Hypertension Reports

, Volume 14, Issue 6, pp 540–547

Striking a Balance: Autophagy, Apoptosis, and Necrosis in a Normal and Failing Heart

  • Wajihah Mughal
  • Rimpy Dhingra
  • Lorrie A. Kirshenbaum
Mediators, Mechanisms, and Pathways in Tissue Injury (B Rothermel, Section Editor)

DOI: 10.1007/s11906-012-0304-5

Cite this article as:
Mughal, W., Dhingra, R. & Kirshenbaum, L.A. Curr Hypertens Rep (2012) 14: 540. doi:10.1007/s11906-012-0304-5

Abstract

Despite the progress that has been made over the past two decades in cardiovascular research, heart failure remains a major cause of morbidity and mortality worldwide. Insight into the cellular and molecular mechanisms that underlie the heart failure in individuals with ischemic heart disease have identified defects in cellular processes that govern autophagy, apoptosis and necrosis as a prevailing underlying cause. Indeed, programmed cell death of cardiac cells by apoptosis or necrosis is believed to involve the intrinsic mitochondrial pathway and/or extrinsic death receptor pathway by certain Bcl-2 family members as well as components of the TNFα signaling pathway. In this review, we discuss recent advances in the molecular signaling factors that govern cardiac cell fate under normal and disease conditions.

Keywords

Heart disease TNFα NF-κB Autophagy Programmed cell death Apoptosis Necrosis RIP1 RIP3 Mitochondria Ubiquitination Necrostatin-1 

Copyright information

© Springer Science+Business Media, LLC 2012

Authors and Affiliations

  • Wajihah Mughal
    • 1
  • Rimpy Dhingra
    • 1
  • Lorrie A. Kirshenbaum
    • 1
    • 2
    • 3
  1. 1.The Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Department of PhysiologyUniversity of ManitobaWinnipegCanada
  2. 2.Faculty of MedicineUniversity of ManitobaWinnipegCanada
  3. 3.Institute of Cardiovascular SciencesSt. Boniface General Hospital Research Centre Rm. 3016WinnipegCanada