Ca2+ toxicity and mitochondrial damage in acute pancreatitis: Translational overview

József Maléth, Péter Hegyi

Research output: Contribution to journalReview article

21 Citations (Scopus)

Abstract

Acute pancreatitis (AP) is a leading cause of hospitalization among nonmalignant gastrointestinal disorders. The mortality of severe AP can reach 30-50%, which is most probably owing to the lack of specific treatment. Therefore, AP is a major healthcare problem, which urges researchers to identify novel drug targets. Studies from the last decades highlighted that the toxic cellular Ca2+ overload and mitochondrial damage are key pathogenic steps in the disease development affecting both acinar and ductal cell functions. Moreover, recent observations showed that modifying the cellular Ca2+ signalling might be beneficial in AP. The inhibition of Ca2+ release from the endoplasmic reticulum or the activity of plasma membrane Ca2+ influx channels decreased the severity of AP in experimental models. Similarly, inhibition of mitochondrial permeability transition pore (MPTP) opening also seems to improve the outcome of AP in in vivo animal models. At the moment MPTP blockers are under detailed clinical investigation to test whether interventions in MPTP openings and/or Ca2+ homeostasis of the cells can be specific targets in prevention or treatment of cell damage in AP. This article is part of the themed issue ‘Evolution brings Ca2+ and ATP together to control life and death’.

Original languageEnglish
Article number20150425
JournalPhilosophical Transactions of the Royal Society B: Biological Sciences
Volume371
Issue number1700
DOIs
Publication statusPublished - Aug 5 2016

Keywords

  • Acute pancreatitis
  • Ca overload
  • Mitochondrial damage

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Agricultural and Biological Sciences(all)

Fingerprint Dive into the research topics of 'Ca<sup>2+</sup> toxicity and mitochondrial damage in acute pancreatitis: Translational overview'. Together they form a unique fingerprint.

  • Cite this