Complex I and II are required for normal mitochondrial Ca2+ homeostasis

Fabian Jaña, G. Bustos, José Rivas, P. Cruz, F. Urra, C. Basualto-Alarcón, Eduardo Sagredo, Melany Ríos, Alenka Lovy, Zhiwei Dong, O. Cerda, Muniswamy Madesh, César Cárdenas

Research output: Contribution to journalArticlepeer-review

16 Scopus citations


Cytosolic calcium (cCa2+) entry into mitochondria is facilitated by the mitochondrial membrane potential (ΔΨm), an electrochemical gradient generated by the electron transport chain (ETC). Is has been assumed that as long as mutations that affect the ETC do not affect the ΔΨm, the mitochondrial Ca2+ (mCa2+) homeostasis remains normal. We show that knockdown of NDUFAF3 and SDHB reduce ETC activity altering mCa2+ efflux and influx rates while ΔΨm remains intact. Shifting the equilibrium toward lower [Ca2+]m accumulation renders cells resistant to death. Our findings reveal an unexpected relationship between complex I and II with the mCa2+ homeostasis independent of ΔΨm.

Original languageEnglish (US)
Pages (from-to)73-82
Number of pages10
StatePublished - Nov 2019


  • Calcium flux
  • Cell death
  • Migration
  • Mitochondrial membrane potential

ASJC Scopus subject areas

  • Molecular Medicine
  • Molecular Biology
  • Cell Biology


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