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Poly(ADP-ribose) makes a date with death

James T Heeres1, Paul J Hergenrother

  • 1Department of Chemistry, Roger Adams Laboratory, University of Illinois, Urbana, IL 61801, USA.

Current Opinion in Chemical Biology
|October 16, 2007
PubMed

Insights

Poly(ADP-ribose) polymerase (PARP) enzymes generate poly(ADP-ribose) (PAR), which triggers cell death by releasing apoptosis-inducing factor (AIF) from mitochondria. This review covers PAR signaling, its role in diseases, and therapeutic targets like PARG and AIF.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Background:

  • Poly(ADP-ribose) polymerase (PARP) enzymes are key regulators of DNA repair pathways.
  • Recent findings highlight a novel role for poly(ADP-ribose) (PAR) in directly inducing mitochondrial cell death.
  • PARP activity influences cellular fate beyond DNA damage response.

Purpose of the Study:

  • To review the synthesis and degradation pathways of poly(ADP-ribose) (PAR).
  • To elucidate the role of PAR misregulation in various disease states.
  • To explore therapeutic interventions targeting PAR signaling, focusing on PARG and AIF.

Main Methods:

  • Literature review of PARP enzymes and poly(ADP-ribose) (PAR) signaling.
  • Analysis of PAR's role in mitochondrial function and cell death.
  • Examination of disease-associated PAR misregulation and therapeutic strategies.

Main Results:

  • PAR directly induces cell death by promoting apoptosis-inducing factor (AIF) release from mitochondria.
  • Dysregulation of PAR synthesis and degradation is implicated in diverse pathologies.
  • Small molecules targeting PAR signaling offer potential therapeutic avenues.

Conclusions:

  • PAR plays a critical role in programmed cell death via mitochondrial pathways.
  • Targeting PAR signaling, particularly PARG and AIF, presents promising therapeutic opportunities for diseases linked to PAR misregulation.

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