ArticleNature communications2022
Mitochondrial calcium uniporter stabilization preserves energetic homeostasis during Complex I impairment.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 33 papers.
What it found
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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.
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Who cites it
33 citing papers in PubMed, 44 citations in OpenAlex.
- Matrix polyamines regulate bidirectional calcium flux through MCU.Structure (London, England : 1993) · 2026Article
- InsP3R signaling and actomyosin-dependent mitochondrial dynamics play essential roles in mitochondrial stress-induced longevity.Nature communications · 2026Article
- Mitochondrial Toxicology of Heavy Metals and Pesticides: Transport Systems, Mitochondrial Dysfunction and Permeability Transition.International journal of molecular sciences · 2026Review
- Mitochondrial Dysfunction: From Molecular Mechanisms to Modern Approaches for Basic and Clinical Research.Biomedicines · 2026Review
- Reconstructing calcium conductance in MCUb illuminates its molecular design for tuning the mitochondrial calcium uniporter.Nature communications · 2026Article
- When calcium calls the shots in FAD-dependent respiration.Nature metabolism · 2026Article
- Chronic cold exposure induces plasticity of mitochondrial calcium uptake in beige and brown fat of UCP1-deficient mice.bioRxiv : the preprint server for biology · 2026Article
- Mitochondrial Calcium Signaling in Hepatocyte Health and Disease.Cold Spring Harbor perspectives in biology · 2026Review
- Disrupted energy metabolism is associated with retinal ganglion cell degeneration in autosomal dominant optic atrophy.Science advances · 2026Article
- InsP3R signaling mediates mitochondrial stress-induced longevity through actomyosin-dependent mitochondrial dynamics.bioRxiv : the preprint server for biology · 2025Article
- Inter-Organellar CaCells · 2025Review
- LONP1 regulation of mitochondrial protein folding provides insight into beta cell failure in type 2 diabetes.Nature metabolism · 2025Article
- Mitochondrial Calcium Uniporter Regulates ITAM-Dependent Platelet Activation.Circulation research · 2025Article
- Mitochondrial calcium signaling regulates branched-chain amino acid catabolism in fibrolamellar carcinoma.Science advances · 2025Article
- Mechanism of MCUB-Dependent Inhibition of Mitochondrial Calcium Uptake.Journal of cellular physiology · 2025Article
- Dependence of mitochondrial calcium signalling and dynamics on the disaggregase, CLPB.Nature communications · 2025Article
- The flexible chain: regulation of structure and activity of ETC complexes defines rate of ATP synthesis and sites of superoxide generation.Biophysical reviews · 2025Review
- Laminin-α2 chain deficiency in skeletal muscle causes dysregulation of multiple cellular mechanisms.Life science alliance · 2024Article
- Mitochondrial membrane lipids in the regulation of bioenergetic flux.Cell metabolism · 2024Review
- Mitochondrial Calcium Regulation of Cardiac Metabolism in Health and Disease.Physiology (Bethesda, Md.) · 2024Review
Corrections and comments
- Erratum issued
Authors and funding
22 authors at 5 institutions in 1 country.
Funding
Abstract
Calcium entering mitochondria potently stimulates ATP synthesis. Increases in calcium preserve energy synthesis in cardiomyopathies caused by mitochondrial dysfunction, and occur due to enhanced activity of the mitochondrial calcium uniporter channel. The signaling mechanism that mediates this compensatory increase remains unknown. Here, we find that increases in the uniporter are due to impairment in Complex I of the electron transport chain. In normal physiology, Complex I promotes uniporter degradation via an interaction with the uniporter pore-forming subunit, a process we term Complex I-induced protein turnover. When Complex I dysfunction ensues, contact with the uniporter is inhibited, preventing degradation, and leading to a build-up in functional channels. Preventing uniporter activity leads to early demise in Complex I-deficient animals. Conversely, enhancing uniporter stability rescues survival and function in Complex I deficiency. Taken together, our data identify a fundamental pathway producing compensatory increases in calcium influx during Complex I impairment.
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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.