ArticleCellular and molecular life sciences : CMLS2019
Mitochondrial stress triggers a pro-survival response through epigenetic modifications of nuclear DNA.
Article in Cellular and molecular life sciences : CMLS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Nutrition, Cell Signalling, Mitochondrial Function, and Chronic Non-Communicable Disease.International journal of molecular sciences · 2026Review
- Mitochondrial DNA methylation is involved in contrast-induced renal tubular epithelial cell injury.Renal failure · 2025Article
- Rewriting nuclear epigenetic scripts in mitochondrial diseases as a strategy for heteroplasmy control.EMBO molecular medicine · 2025Article
- Aspects of β-sitosterol's Pharmacology, Nutrition and Analysis.Current pharmaceutical biotechnology · 2025Review
- Ionizing radiations induce shared epigenomic signatures unraveling adaptive mechanisms of cancerous cell lines with or without methionine dependency.Clinical epigenetics · 2021Article
- Clinical and molecular characterization of mitochondrial DNA disorders in a group of Argentinian pediatric patients.Molecular genetics and metabolism reports · 2021Article
- The effect of mitochondrial transplantation therapy from different gender on inhibiting cell proliferation of malignant melanoma.International journal of biological sciences · 2021Article
- Structure, mechanism, and regulation of mitochondrial DNA transcription initiation.The Journal of biological chemistry · 2020Review
- Hippocampal tau oligomerization early in tau pathology coincides with a transient alteration of mitochondrial homeostasis and DNA repair in a mouse model of tauopathy.Acta neuropathologica communications · 2020Article
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction represents an important cellular stressor and when intense and persistent cells must unleash an adaptive response to prevent their extinction. Furthermore, mitochondria can induce nuclear transcriptional changes and DNA methylation can modulate cellular responses to stress. We hypothesized that mitochondrial dysfunction could trigger an epigenetically mediated adaptive response through a distinct DNA methylation patterning. We studied cellular stress responses (i.e., apoptosis and autophagy) in mitochondrial dysfunction models. In addition, we explored nuclear DNA methylation in response to this stressor and its relevance in cell survival. Experiments in cultured human myoblasts revealed that intense mitochondrial dysfunction triggered a methylation-dependent pro-survival response. Assays done on mitochondrial disease patient tissues showed increased autophagy and enhanced DNA methylation of tumor suppressor genes and pathways involved in cell survival regulation. In conclusion, mitochondrial dysfunction leads to a "pro-survival" adaptive state that seems to be triggered by the differential methylation of nuclear genes.
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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.