4.3 Article

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

Journal

CURRENT HYPERTENSION REPORTS
Volume 14, Issue 6, Pages 540-547

Publisher

SPRINGER
DOI: 10.1007/s11906-012-0304-5

Keywords

Heart disease; TNF alpha; NF-kappa B; Autophagy; Programmedcell death; Apoptosis; Necrosis; RIP1; RIP3; Mitochondria; Ubiquitination; Necrostatin-1

Funding

  1. Manitoba Health Research Council
  2. Canadian Institutes of Health Research
  3. Heart and Stroke Foundation

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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 TNF alpha signaling pathway. In this review, we discuss recent advances in the molecular signaling factors that govern cardiac cell fate under normal and disease conditions.

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