ReviewBrain pathology (Zurich, Switzerland)2022
The epigenetic mechanisms involved in mitochondrial dysfunction: Implication for Parkinson's disease.
Review in Brain pathology (Zurich, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed.
- Convergent transcriptomic signature in iPSC-dopaminergic neurons of hereditary Parkinson's disease.Life science alliance · 2026Article
- Multi-omics approaches to parkinsonism: genomic, proteomic, and non-coding RNA perspectives.Molecular biology reports · 2026Review
- Mitochondrial-Based Nanomedicine in Treatment of Liver Cancer.Molecular biotechnology · 2026Review
- Phosphorylated ubiquitin is a secondary messenger and an epigenetic mark mediating mitochondria to nucleus signaling.bioRxiv : the preprint server for biology · 2026Article
- Parkinson's disease: pathogenesis and therapeutic strategies.Molecular biomedicine · 2026Review
- The Interplay Between Nurr1 and Mitochondrial Biogenesis: Implications for Neurodegenerative Therapy.Molecular neurobiology · 2026Review
- Nuclear receptors in metabolic, inflammatory, and oncologic diseases: mechanisms, therapeutic advances, and future directions.European journal of medical research · 2025Review
- Epigenetic Regulation of Aging and its Rejuvenation.MedComm · 2025Review
- Epigenetic and Mitochondrial Metabolic Dysfunction in Multiple Sclerosis: A Review of Herbal Drug Approaches and Current Clinical Trials.Molecular neurobiology · 2025Review
- Epigenetic Dysregulation in Neurodegenerative Disease: Implications for Neuropathology and Therapy.Cureus · 2025Review
- Evidence based molecular pathways, available drug targets, pre- clinical animal models and future disease modifying treatments of huntington's disease.Molecular biology reports · 2025Review
- Genomic ncRNAs regulating mitochondrial function in neurodegeneration: a neglected clue in the complex etiopathogenesis of multiple sclerosis.Cell & bioscience · 2025Article
- Reversing Epigenetic Dysregulation in Neurodegenerative Diseases: Mechanistic and Therapeutic Considerations.International journal of molecular sciences · 2025Review
- Unravelling the Proteinopathic Engagement of α-Synuclein, Tau, and Amyloid Beta in Parkinson's Disease: Mitochondrial Collapse as a Pivotal Driver of Neurodegeneration.Neurochemical research · 2025Review
- Loss of MEF2C function by enhancer mutation leads to neuronal mitochondria dysfunction and motor deficits in mice.Molecular neurodegeneration · 2025Article
- Nano-structured strategies in combatting neurodegeneration.Frontiers in bioengineering and biotechnology · 2025Review
- Peripheral-central immune interactions in Parkinson's disease: insights into innate and adaptive immunity.Frontiers in molecular neuroscience · 2025Review
- Immune aging and infectious diseases.Chinese medical journal · 2024Review
- Epigenetic reprogramming of mtDNA and its etiology in mitochondrial diseases.Journal of physiology and biochemistry · 2024Review
- Retinal G-protein-coupled receptor deletion exacerbates AMD-like changes via the PINK1-parkin pathway under oxidative stress.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction is one of the crucial factors involved in PD's pathogenicity, which emerges from a combination of genetic and environmental factors. These factors cause differential molecular expression in neurons, such as varied transcriptional regulation of genes, elevated oxidative stress, α-synuclein aggregation and endogenous neurotoxins release, which induces epigenetic modifications and triggers energy crisis by damaging mitochondria of the dopaminergic neurons (DN). So far, these events establish a complicated relationship with underlying mechanisms of mitochondrial anomalies in PD, which has remained unclear for years and made PD diagnosis and treatment extremely difficult. Therefore, in this review, we endeavored to discuss the complex association of epigenetic modifications and other associated vital factors in mitochondrial dysfunction. We propose a hypothesis that describes a vicious cycle in which mitochondrial dysfunction and oxidative stress act as a hub for regulating DA neuron's fate in PD. Oxidative stress triggers the release of endogenous neurotoxins (CTIQs) that lead to mitochondrial dysfunction along with abnormal α-synuclein aggregation and epigenetic modifications. These disturbances further intensify oxidative stress and mitochondrial damage, amplifying the synthesis of CTIQs and works vice versa. This vicious cycle may result in the degeneration of DN to hallmark Parkinsonism. Furthermore, we have also highlighted various endogenous compounds and epigenetic marks (neurotoxic and neuroprotective), which may help for devising future diagnostic biomarkers and target specific drugs using novel PD management strategies.
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