Experiments reveal ATAD3's role in mitochondrial permeability transition pore in cardiomyocytes, highlighting its critical function.
Our recent collaborative studies (Robichaux et al., bioRxiv [Preprint] 2025 doi: 10.1101/2025.06.13.658955) identify ATAD3a as a critical component of the mitochondrial permeability transition pore (mPTP). Here, we highlight patch-clamp recordings of recombinant ATAD3a reconstituted in liposomes, which reveal intrinsic channel activity consistent with pore formation. Complementarily, genetic deletion of Atad3 in cardiomyocytes and hepatocytes produced mitochondria with dramatically increased calcium retention capacity and resistance to permeability transition and swelling. Together, these findings provide electrophysiological and functional evidence supporting ATAD3a as an essential pore-forming element of the mPTP.
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Lopez et al. (2026) studied this question.
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