ReviewHuman genetics2014
The emergence of the mitochondrial genome as a partial regulator of nuclear function is providing new insights into the genetic mechanisms underlying age-related complex disease.
Review in Human genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 44 citations in OpenAlex.
- Review
- Mitochondrial gene expression signature predicts prognosis of pediatric acute myeloid leukemia patients.Frontiers in oncology · 2023Article
- Article
- mtDNA haplogroup A enhances the effect of obesity on the risk of knee OA in a Mexican population.Scientific reports · 2022Article
- Ovarian Aging: Role of Pituitary-Ovarian Axis Hormones and ncRNAs in Regulating Ovarian Mitochondrial Activity.Frontiers in endocrinology · 2021Review
- Mitochondrial DNA in osteoarthritis disease.Clinical rheumatology · 2020Article
- Mitochondrial DNA copy number can influence mortality and cardiovascular disease via methylation of nuclear DNA CpGs.Genome medicine · 2020Article
- Estrogenic control of mitochondrial function.Redox biology · 2020Review
- Mitochondrial Genetics and Epigenetics in Osteoarthritis.Frontiers in genetics · 2019Review
- Mitochondrial DNA variation and the pathogenesis of osteoarthritis phenotypes.Nature reviews. Rheumatology · 2018Review
- Knockout of Mpv17-Like Protein (M-LPH) Gene in Human Hepatoma Cells Results in Impairment of mtDNA Integrity through Reduction of TFAM, OGG1, and LIG3 at the Protein Levels.Oxidative medicine and cellular longevity · 2018Article
- Mitochondrial Genomic Backgrounds Affect Nuclear DNA Methylation and Gene Expression.Cancer research · 2017Article
- Mitochondrial DNA variants in colorectal carcinogenesis: Drivers or passengers?Journal of cancer research and clinical oncology · 2017Review
- Estrogens regulate life and death in mitochondria.Journal of bioenergetics and biomembranes · 2017Review
- Mitochondrial genetic haplogroups and depressive symptoms: A large study among people in North America.Journal of affective disorders · 2017Article
- Nuclear respiratory factor-1 and bioenergetics in tamoxifen-resistant breast cancer cells.Experimental cell research · 2016Article
- Mitochondrial variants in MT-CO2 and D-loop instability are involved in MUTYH-associated polyposis.Journal of molecular medicine (Berlin, Germany) · 2015Article
- Inherited mtDNA variations are not strong risk factors in human prion disease.Neurobiology of aging · 2015Article
- Mitonuclear linkage disequilibrium in human populations.Proceedings. Biological sciences · 2015Article
- Human genetics' 50th anniversary issue.Human genetics · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial malfunction appears to be intimately associated with age and age-related complex disorders but the precise pathological relevance of such malfunction remains unclear. Mitochondrial, and more specifically bioenergetic, malfunction is commonly encountered in cancer, degenerative disorders and aging. The identification of a mitochondrial-nuclear retrograde signaling pathway in yeast has facilitated the study of the corresponding retrograde signaling mechanisms induced in response to mitochondrial malfunction in mammals including human. Mitochondrial-nuclear crosstalk is critical for the maintenance of cellular homeostasis, and some mitochondrial DNA mutations may perturb crosstalk signaling. However, ascertaining whether mitochondrial malfunction is a cause or a consequence of disease development will be key to determining whether or not impaired crosstalk signaling is of direct pathological and hence therapeutic relevance. Here, we review what is known about the nuclear adaptive compensatory mechanisms induced in response to mitochondrial malfunction. We discuss the role of mitochondrial DNA variants in modulating the penetrance of human inherited disease caused by mutations in the nuclear genome and explore the underlying mechanisms by which they influence the retrograde response. We conclude that mitochondrial DNA variants have the potential to induce molecular signals through the mitochondrial-nuclear crosstalk mechanism, thereby promoting nuclear compensation in response to mitochondrial malfunction. The implications for the development of genetic or pharmaceutical interventions for the treatment of mitochondrial malfunction in complex disease are also explored.
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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.