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@ARTICLE{Vetralla:284337,
      author       = {Vetralla, Massimo and Wischhof, Lena and Kahsay, Asrat and
                      Cadenelli, Vanessa and Scifo, Enzo and Xie, Beijia and
                      Sbrissa, Miriana and Habert, Maelle and Ehninger, Dan and
                      Rizzuto, Rosario and Bano, Daniele and De Stefani, Diego},
      title        = {{TMEM}65-dependent {C}a2+ extrusion safeguards
                      mitochondrial homeostasis.},
      journal      = {Nature Communications},
      volume       = {17},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {DZNE-2026-00112},
      pages        = {923},
      year         = {2025},
      abstract     = {The bidirectional transport of Ca2+ into and out of
                      mitochondria regulates metabolism, signaling, and cell fate.
                      While influx is mediated by the Mitochondrial Calcium
                      Uniporter (MCU) complex, efflux mechanisms are more
                      diversified, involving Na⁺ or H⁺ exchange pathways. We
                      here demonstrate that TMEM65 is a fundamental component of
                      the Ca2+ efflux machinery of mitochondria. Its
                      overexpression specifically enhances Na⁺- and
                      Li⁺-dependent mitochondrial Ca²⁺ extrusion. This effect
                      is inhibited by CGP-37157 and does not depends on NCLX,
                      currently considered the bona fide mitochondrial Na+/Ca2+
                      exchanger. Its downregulation chronically elevates basal
                      [Ca²⁺]mt and impairs efflux upon stimulation. In
                      Caenorhabditis elegans, deletion of TMEM65 homologs
                      compromises embryonic development under mild thermal stress,
                      causing necrotic lesions that are suppressed by genetic
                      inhibition of MCU-1. These findings highlight a molecular
                      component that may be relevant in pathological settings in
                      which excessive mitochondrial Ca2+ accumulation critically
                      contribute to degenerative pathways.},
      keywords     = {Animals / Mitochondria: metabolism / Caenorhabditis
                      elegans: metabolism / Caenorhabditis elegans: genetics /
                      Calcium: metabolism / Homeostasis / Caenorhabditis elegans
                      Proteins: metabolism / Caenorhabditis elegans Proteins:
                      genetics / Membrane Proteins: metabolism / Membrane
                      Proteins: genetics / Calcium Channels: metabolism / Calcium
                      Channels: genetics / Clonazepam: analogs $\&$ derivatives /
                      Clonazepam: pharmacology / Sodium-Calcium Exchanger:
                      metabolism / Sodium-Calcium Exchanger: genetics / Humans /
                      Mitochondrial Proteins: metabolism / Mitochondrial Proteins:
                      genetics / Thiazepines / Calcium (NLM Chemicals) /
                      Caenorhabditis elegans Proteins (NLM Chemicals) / Membrane
                      Proteins (NLM Chemicals) / Calcium Channels (NLM Chemicals)
                      / Clonazepam (NLM Chemicals) / mitochondrial calcium
                      uniporter (NLM Chemicals) / Sodium-Calcium Exchanger (NLM
                      Chemicals) / CGP 37157 (NLM Chemicals) / Mitochondrial
                      Proteins (NLM Chemicals) / Thiazepines (NLM Chemicals)},
      cin          = {AG Bano / AG Ehninger},
      ddc          = {500},
      cid          = {I:(DE-2719)1013003 / I:(DE-2719)1013005},
      pnm          = {351 - Brain Function (POF4-351) / 352 - Disease Mechanisms
                      (POF4-352)},
      pid          = {G:(DE-HGF)POF4-351 / G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41408045},
      pmc          = {pmc:PMC12830682},
      doi          = {10.1038/s41467-025-67647-y},
      url          = {https://pub.dzne.de/record/284337},
}