Calcium and mitochondrial metabolism in ceramide-induced cardiomyocyte death

Valentina Parra, Francisco Moraga, Jovan Kuzmicic, Camila López-Crisosto, Rodrigo Troncoso, Natalia Torrealba, Alfredo Criollo, Jessica Díaz-Elizondo, Beverly A. Rothermel, Andrew F G Quest, Sergio Lavandero

Research output: Contribution to journalArticlepeer-review

37 Scopus citations


Ceramides are important intermediates in the biosynthesis and degradation of sphingolipids that regulate numerous cellular processes, including cell cycle progression, cell growth, differentiation and death. In cardiomyocytes, ceramides induce apoptosis by decreasing mitochondrial membrane potential and promoting cytochrome-c release. Ca2+ overload is a common feature of all types of cell death. The aim of this study was to determine the effect of ceramides on cytoplasmic Ca2+ levels, mitochondrial function and cardiomyocyte death. Our data show that C2-ceramide induces apoptosis and necrosis in cultured cardiomyocytes by a mechanism involving increased Ca2+ influx, mitochondrial network fragmentation and loss of the mitochondrial Ca2+ buffer capacity. These biochemical events increase cytosolic Ca2+ levels and trigger cardiomyocyte death via the activation of calpains.

Original languageEnglish (US)
Pages (from-to)1334-1344
Number of pages11
JournalBiochimica et Biophysica Acta - Molecular Basis of Disease
Issue number8
StatePublished - Aug 2013


  • Ca
  • Cardiomyocyte
  • Cell death
  • Ceramide
  • Metabolism
  • Mitochondrial dynamics

ASJC Scopus subject areas

  • Molecular Medicine
  • Molecular Biology


Dive into the research topics of 'Calcium and mitochondrial metabolism in ceramide-induced cardiomyocyte death'. Together they form a unique fingerprint.

Cite this