ArticleScience advances2020
Mitochondria form contact sites with the nucleus to couple prosurvival retrograde response.
Article in Science advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 2 of them syntheses that pooled it.
What it found
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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
106 citing papers in PubMed, 2 syntheses or guidelines pooled it, 151 citations in OpenAlex.
- Stay in touch with the endoplasmic reticulum.Science China. Life sciences · 2024Pooled it
- Mitochondrial Proteomes in Neural Cells: A Systematic Review.Biomolecules · 2023Pooled it
- Dual inhibition of SGLT 1 and 2 by sotagliflozin alleviates intracellular sodium overload and improves cardiometabolic remodelling in uraemic cardiomyopathy.Cardiovascular research · 2026Article
- Metabolites with a message: impacts on epigenetics and implications for epimetabopathies.EMBO reports · 2026Review
- Spatial architecture of immunometabolism: Mitochondrial‑organelle interfaces in immune signaling (Review).International journal of molecular medicine · 2026Review
- Spatial control of mitochondrial retrograde signaling by nuclear pore-associated contact sites.bioRxiv : the preprint server for biology · 2026Article
- From Adaptive Resilience to Catastrophic Systems Collapse: Endothelial Entropy, Ferroptotic Propagation, and the Maternal Point of No Return in Emergency Peripartum Hysterectomy.International journal of molecular sciences · 2026Review
- Dissecting mitochondria-nucleus contact sites using SPLICS reveals a distributed and dynamic tethering network.Biology direct · 2026Article
- Getting nuclear size just right - emerging mechanisms regulating nuclear scaling and morphology.Journal of cell science · 2026Review
- Beyond the Powerhouse: Mitochondrial Crosstalk as a Master Regulator of Cardiac Metabolic Homeostasis and Failure.Journal of cardiovascular translational research · 2026Review
- Organelle contact sites in cancer cells.Cell death & disease · 2026Review
- F2,6BP restores mitochondrial genome integrity in Huntington's disease.The Journal of biological chemistry · 2026Article
- A central role for PINK1 in governing local mitochondrial biogenesis and degradation in neurons.Cellular and molecular life sciences : CMLS · 2026Review
- Astaxanthin improves myogenicity of aged skeletal muscle progenitor cells in a sexually dimorphic manner.npj aging · 2026Article
- Stress-induced mitochondrial fragmentation in endothelial cells disrupts blood-retinal barrier integrity causing neurodegeneration.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- C-COMPASS: a user-friendly neural network tool profiles cell compartments at protein and lipid levels.Nature methods · 2026Article
- Mitochondria-derived vesicles serve as reactors in response to stress in cardiomyocytes.Cell communication and signaling : CCS · 2025Article
- Critical role of translocator protein (TSPO) in neuronal mitochondrial dysfunction and mental stress-exacerbated ischemic injury following stroke.Translational psychiatry · 2025Article
- TCA-cycle metabolites in the nucleus: drivers of chromatin and epigenetic control.BMC biology · 2025Review
- A Perspective on the Role of Metformin in Treating Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Long COVID.ACS pharmacology & translational science · 2025Review
46 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
24 authors at 8 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria drive cellular adaptation to stress by retro-communicating with the nucleus. This process is known as mitochondrial retrograde response (MRR) and is induced by mitochondrial dysfunction. MRR results in the nuclear stabilization of prosurvival transcription factors such as the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). Here, we demonstrate that MRR is facilitated by contact sites between mitochondria and the nucleus. The translocator protein (TSPO) by preventing the mitophagy-mediated segregation o mitochonria is required for this interaction. The complex formed by TSPO with the protein kinase A (PKA), via the A-kinase anchoring protein acyl-CoA binding domain containing 3 (ACBD3), established the tethering. The latter allows for cholesterol redistribution of cholesterol in the nucleus to sustain the prosurvival response by blocking NF-κB deacetylation. This work proposes a previously unidentified paradigm in MRR: the formation of contact sites between mitochondria and nucleus to aid communication.
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.