Signaling pathways that protect the heart against apoptosis induced by ischemia and reperfusion

Zheqing Cai, Gregg L. Semenza

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Ischemia and reperfusion injury commonly occurs in ischemic heart disease, resulting in apoptotic or necrotic cell death. Apoptotic cell death is highly regulated. Two mechanisms of apoptosis involve the extrinsic death receptor pathway and the intrinsic mitochondrial pathway. Both pathways lead to the activation of effector caspases, resulting in cell death. The mitochondrial pathway plays a key role in initiating apoptosis after ischemia and reperfusion. The phosphatidylinositol 3-kinase (PI3K), protein kinase C (PKC), and extracellular signal-regulated kinase (ERK) signaling pathways protect the heart against ischemia and reperfusion injury. They inhibit mitochondrial cytochrome c release into the cytosol by regulating the Bcl-2 family proteins and activating the mitoKATP channel, thereby blocking the process of apoptosis.

Original languageEnglish (US)
Title of host publicationApoptosis, Cell Signaling, and Human Diseases
PublisherHumana Press
Pages181-195
Number of pages15
Volume2
ISBN (Print)1588296776, 9781588296771
DOIs
StatePublished - Dec 1 2007

Keywords

  • Apoptosis
  • Bcl-2
  • ERK
  • PI3K
  • PKC
  • cardioprotection
  • caspases
  • ischemia and reperfusion injury
  • mitochondria
  • signal transduction

ASJC Scopus subject areas

  • Medicine(all)
  • Biochemistry, Genetics and Molecular Biology(all)

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