ArticleNature communications2022
Mechanical instability generated by Myosin 19 contributes to mitochondria cristae architecture and OXPHOS.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed.
- Revisiting Alzheimer's Disease Through the Somatostatin-Mitochondria Axis.Molecular neurobiology · 2026Review
- MICOS and MIMAS, multifunctional assemblies linking mitochondrial biogenesis, architecture, and function.Protein science : a publication of the Protein Society · 2026Review
- Dynamic Proximity Networks of Myosin-19 (Myo19) and its Mitochondrial Receptors Miro2 and Metaxin-3.Molecular & cellular proteomics : MCP · 2026Article
- ICAM2 promotes endocrine resistance via dynein-mediated OXPHOS activation in ER-positive breast cancer.Cell death & disease · 2026Article
- Geometry-programmed self-wrinkling in organo-hydrogels for anisotropic mechanics and adaptive sensing.Nature communications · 2026Article
- Mitochondrial Adaptation to Mechanical Stress in Cardiac Ageing and Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Mitochondrial cristae remodeling: Mechanisms, functions, and pathology.Cell insight · 2025Review
- Article
- Identification of novel MYO19 variants in neonatal hypertrophic cardiomyopathy: a familial analysis revealing oligogenic contributors to disease severity.Orphanet journal of rare diseases · 2025Article
- ER-induced PERK/TFEB cascade sequentially modulates mitochondrial dynamics during cranial suture expansion.Bone research · 2025Article
- Mitochondrial Maintenance in Skeletal Muscle.Cold Spring Harbor perspectives in biology · 2025Review
- Regulation of mitochondrial cristae organization by Myo19, Miro1 and Miro2, and metaxin 3.Journal of cell science · 2025Article
- Compositionally unique mitochondria in filopodia support cellular migration.Current biology : CB · 2025Article
- Identification of Potential Causal Genes for Neurodegenerative Diseases by Mitochondria-Related Genome-Wide Mendelian Randomization.Molecular neurobiology · 2025Article
- Mitochondrial membrane synthesis, remodelling and cellular trafficking.Journal of inherited metabolic disease · 2025Review
- MYO19 is associated with tumor progression, immune evasion, ferroptosis-related signatures in lung squamous cell carcinoma.Frontiers in oncology · 2025Article
- Molecular characterization of human HSPCs with different cell fates in vivo using single-cell transcriptome analysis and lentiviral barcoding technology.Clinical and translational medicine · 2024Article
- The movement of mitochondria in breast cancer: internal motility and intercellular transfer of mitochondria.Clinical & experimental metastasis · 2024Review
- SETD3 is a mechanosensitive enzyme that methylates actin on His73 to regulate mitochondrial dynamics and function.Journal of cell science · 2024Article
- Compositionally unique mitochondria in filopodia support cellular migration.bioRxiv : the preprint server for biology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The folded mitochondria inner membrane-cristae is the structural foundation for oxidative phosphorylation (OXPHOS) and energy production. By mechanically simulating mitochondria morphogenesis, we speculate that efficient sculpting of the cristae is organelle non-autonomous. It has long been inferred that folding requires buckling in living systems. However, the tethering force for cristae formation and regulation has not been identified. Combining electron tomography, proteomics strategies, super resolution live cell imaging and mathematical modeling, we reveal that the mitochondria localized actin motor-myosin 19 (Myo19) is critical for maintaining cristae structure, by associating with the SAM-MICOS super complex. We discover that depletion of Myo19 or disruption of its motor activity leads to altered mitochondria membrane potential and decreased OXPHOS. We propose that Myo19 may act as a mechanical tether for effective ridging of the mitochondria cristae, thus sustaining the energy homeostasis essential for various cellular functions.
Indexed as
Identifiers
What OpenQuestion holds
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.