ArticleLife science alliance2022
TMBIM5 loss of function alters mitochondrial matrix ion homeostasis and causes a skeletal myopathy.
Article in Life science alliance, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
- Loss of TMEM65 in mice causes mitochondrial disease mediated by mitochondrial CaNature communications · 2026Article
- Mitochondrial Calcium Signaling in Hepatocyte Health and Disease.Cold Spring Harbor perspectives in biology · 2026Review
- Tmbim5 and Slc8b1 cooperate in tissue-specific mitochondrial calcium regulation in zebrafish.Communications biology · 2026Article
- Interaction of the mitochondrial calcium/proton exchanger TMBIM5 with MICU1.Communications biology · 2025Article
- Mitochondrial CaJournal of cellular physiology · 2025Review
- The roles of mitochondria in global and local intracellular calcium signalling.Nature reviews. Molecular cell biology · 2025Review
- How does mitochondrial Ca2+ change during ischemia and reperfusion? Implications for activation of the permeability transition pore.The Journal of general physiology · 2025Review
- Systematic mapping of mitochondrial calcium uniporter channel (MCUC)-mediated calcium signaling networks.The EMBO journal · 2024Article
- DELE1 maintains muscle proteostasis to promote growth and survival in mitochondrial myopathy.The EMBO journal · 2024Article
- Mitochondrial Calcium Regulation of Cardiac Metabolism in Health and Disease.Physiology (Bethesda, Md.) · 2024Review
- Mitochondrial calcium uniporter channel gatekeeping in cardiovascular disease.Nature cardiovascular research · 2024Review
- MCU-independent CaScientific reports · 2024Article
- DELE1 promotes translation-associated homeostasis, growth, and survival in mitochondrial myopathy.bioRxiv : the preprint server for biology · 2024Article
- ATF4 Signaling in HIV-1 Infection: Viral Subversion of a Stress Response Transcription Factor.Biology · 2024Review
- Mitochondrial Cation Signalling in the Control of Inflammatory Processes.International journal of molecular sciences · 2023Review
- Beyond the TCA cycle: new insights into mitochondrial calcium regulation of oxidative phosphorylation.Biochemical Society transactions · 2023Review
- Increased mitochondrial free CaCell reports · 2023Article
- The role of CaCell calcium · 2023Review
- Simultaneous Measurement of Changes in Mitochondrial and Endoplasmic Reticulum Free Calcium in Pancreatic Beta Cells.Biosensors · 2023Article
- Preserving and enhancing mitochondrial function after stroke to protect and repair the neurovascular unit: novel opportunities for nanoparticle-based drug delivery.Frontiers in cellular neuroscience · 2023Review
Corrections and comments
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Authors and funding
21 authors at 6 institutions in 5 countries.
Funding
Abstract
Ion fluxes across the inner mitochondrial membrane control mitochondrial volume, energy production, and apoptosis. TMBIM5, a highly conserved protein with homology to putative pH-dependent ion channels, is involved in the maintenance of mitochondrial cristae architecture, ATP production, and apoptosis. Here, we demonstrate that overexpressed TMBIM5 can mediate mitochondrial calcium uptake. Under steady-state conditions, loss of TMBIM5 results in increased potassium and reduced proton levels in the mitochondrial matrix caused by attenuated exchange of these ions. To identify the in vivo consequences of TMBIM5 dysfunction, we generated mice carrying a mutation in the channel pore. These mutant mice display increased embryonic or perinatal lethality and a skeletal myopathy which strongly correlates with tissue-specific disruption of cristae architecture, early opening of the mitochondrial permeability transition pore, reduced calcium uptake capability, and mitochondrial swelling. Our results demonstrate that TMBIM5 is an essential and important part of the mitochondrial ion transport system machinery with particular importance for embryonic development and muscle function.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.