ReviewOxidative medicine and cellular longevity2015
Mitochondrial Retrograde Signaling: Triggers, Pathways, and Outcomes.
Review in Oxidative medicine and cellular longevity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 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
84 citing papers in PubMed, 164 citations in OpenAlex.
- Cancer-associated mitochondrial homeostasis disrupted and retrograde signaling activated.Medical oncology (Northwood, London, England) · 2026Review
- Carbon source-driven metabolic and regulatory remodeling defines phenomic states in Lipomyces starkeyi.Scientific reports · 2026Article
- Small but mighty: mitochondrial DNA at the centre of retrograde signalling.Cell communication and signaling : CCS · 2026Review
- Mitochondrial Long Non-Coding RNAs in Gynecological Cancers: Pathogenic Signaling Pathways and Therapeutic Opportunities.Current issues in molecular biology · 2026Review
- Busulfan resistance in AML is associated with changes in mitochondrial copy number and lipid metabolism.Scientific reports · 2026Article
- Neuro-lymphaphotonics opens new horizons of the future technologies for the therapy of brain diseases.Theranostics · 2026Review
- Nanoscale biointerfaces in inter-organelle communication: membrane contact sites, organelle trafficking, and cell fate control.Frontiers in cell and developmental biology · 2026Review
- NO-ergic mechanisms of age differences in photostimulation of lymphatic drainage, filtration, and clearance.Biomedical optics express · 2025Article
- Lipophilic Cations as Mitochondria-Targeting Moieties: Recent Progress and Design Principles for Medicinal Chemistry.Journal of medicinal chemistry · 2025Review
- Molecular Adaptations to Repeated Radiation Exposure in Triple-Negative Breast Cancer: Dysregulation of Cell Adhesion, Mitochondrial Function, and Epithelial-Mesenchymal Transition.International journal of molecular sciences · 2025Article
- Temporal analysis of doxorubicin-induced cardiac toxicity and hypertrophy.NPJ systems biology and applications · 2025Article
- Endometrial Aging and Reproductive Decline: The Central Role of Mitochondrial Dysfunction.International journal of molecular sciences · 2025Review
- ModulatingBiomolecules · 2024Article
- The correlation between mitochondrial derived peptide (MDP) and metabolic states: a systematic review and meta-analysis.Diabetology & metabolic syndrome · 2024Review
- Exercise-Regulated Mitochondrial and Nuclear Signalling Networks in Skeletal Muscle.Sports medicine (Auckland, N.Z.) · 2024Review
- Mitochondrial-Stem Cell Connection: Providing Additional Explanations for Understanding Cancer.Metabolites · 2024Article
- Beneficial Effects of Low-Grade Mitochondrial Stress on Metabolic Diseases and Aging.Yonsei medical journal · 2024Review
- Neo-functionalization inRoyal Society open science · 2023Article
- Copy number variation alters local and global mutational tolerance.Genome research · 2023Article
- RNA binding protein: coordinated expression between the nuclear and mitochondrial genomes in tumors.Journal of translational medicine · 2023Review
24 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
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria are essential organelles for eukaryotic homeostasis. Although these organelles possess their own DNA, the vast majority (>99%) of mitochondrial proteins are encoded in the nucleus. This situation makes systems that allow the communication between mitochondria and the nucleus a requirement not only to coordinate mitochondrial protein synthesis during biogenesis but also to communicate eventual mitochondrial malfunctions, triggering compensatory responses in the nucleus. Mitochondria-to-nucleus retrograde signaling has been described in various organisms, albeit with differences in effector pathways, molecules, and outcomes, as discussed in this review.
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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.