Inhibition of TRPM2 function by PARP inhibitors protects cells from oxidative stress-induced death

Research output: Contribution to journalReview article

21 Scopus citations

Abstract

TRPM2 is a member of the transient receptor potential (TRP) protein superfamily of calcium-permeable, voltage-independent ion channels expressed in nonexcitable cells. Activation of TRPM2 by oxidative stress results in calcium influx and susceptibility to cell death, whereas inhibition of TRPM2 function enhances cell survival. In the present edition of this journal, Fonfria et al. demonstrate a role for poly(ADP ribose) polymerase (PARP) as a mediator between oxidative stress and TRPM2 activation. They present evidence that inhibition of either PARP or TRPM2 protects cells from plasma membrane damage and cell death. The therapeutic implications of this important observation are discussed.

Original languageEnglish (US)
Pages (from-to)515-516
Number of pages2
JournalBritish Journal of Pharmacology
Volume143
Issue number5
DOIs
StatePublished - Nov 1 2004

All Science Journal Classification (ASJC) codes

  • Pharmacology

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