ArticleAging2019
Mitochondrial and autophagic alterations in skin fibroblasts from Parkinson disease patients with Parkin mutations.
Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- Review
- Multimodal assessment of mitochondrial function in Parkinson's disease.Brain : a journal of neurology · 2024Article
- Parallel neurodegenerative phenotypes in sporadic Parkinson's disease fibroblasts and midbrain dopamine neurons.Progress in neurobiology · 2023Article
- Molecular phenotypes of mitochondrial dysfunction in clinically non-manifesting heterozygous PRKN variant carriers.NPJ Parkinson's disease · 2023Article
- Unravelling inclusion body myositis using a patient-derived fibroblast model.Journal of cachexia, sarcopenia and muscle · 2023Article
- Monoterpenoid Epoxidiol Ameliorates the Pathological Phenotypes of the Rotenone-Induced Parkinson's Disease Model by Alleviating Mitochondrial Dysfunction.International journal of molecular sciences · 2023Article
- Regulators of proteostasis are translationally repressed in fibroblasts from patients with sporadic and LRRK2-G2019S Parkinson's disease.NPJ Parkinson's disease · 2023Article
- The use of fibroblasts as a valuable strategy for studying mitochondrial impairment in neurological disorders.Translational neurodegeneration · 2022Review
- Bioenergetic and Autophagic Characterization of Skin Fibroblasts fromAntioxidants (Basel, Switzerland) · 2022Article
- Growth factors-based platelet lysate rejuvenates skin against ageing through NF-κB signalling pathway: In vitro and in vivo mechanistic and clinical studies.Cell proliferation · 2022Article
- Article
- Mitochondrial Inorganic Polyphosphate (polyP) Is a Potent Regulator of Mammalian Bioenergetics in SH-SY5Y Cells: A Proteomics and Metabolomics Study.Frontiers in cell and developmental biology · 2022Article
- Transcriptome analysis in LRRK2 and idiopathic Parkinson's disease at different glucose levels.NPJ Parkinson's disease · 2021Article
- Parkin, an E3 Ubiquitin Ligase, Plays an Essential Role in Mitochondrial Quality Control in Parkinson's Disease.Cellular and molecular neurobiology · 2021Review
- Synergistic Effects of Milk-Derived Exosomes and Galactose onInternational journal of molecular sciences · 2021Review
- Multitasking guardian of mitochondrial quality: Parkin function and Parkinson's disease.Translational neurodegeneration · 2021Review
- Disrupted Mitochondrial and Metabolic Plasticity Underlie Comorbidity between Age-Related and Degenerative Disorders as Parkinson Disease and Type 2 Diabetes Mellitus.Antioxidants (Basel, Switzerland) · 2020Article
- Mitochondrial Dysfunction: A Common Hallmark Underlying Comorbidity between sIBM and Other Degenerative and Age-Related Diseases.Journal of clinical medicine · 2020Article
- Galactose-Induced Skin Aging: The Role of Oxidative Stress.Oxidative medicine and cellular longevity · 2020Review
- Autophagic- and Lysosomal-Related Biomarkers for Parkinson's Disease: Lights and Shadows.Cells · 2019Review
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PRKN encodes an E3-ubiquitin-ligase involved in multiple cell processes including mitochondrial homeostasis and autophagy. Previous studies reported alterations of mitochondrial function in fibroblasts from patients with PRKN mutation-associated Parkinson's disease (PRKN-PD) but have been only conducted in glycolytic conditions, potentially masking mitochondrial alterations. Additionally, autophagy flux studies in this cell model are missing.We analyzed mitochondrial function and autophagy in PRKN-PD skin-fibroblasts (n=7) and controls (n=13) in standard (glucose) and mitochondrial-challenging (galactose) conditions.In glucose, PRKN-PD fibroblasts showed preserved mitochondrial bioenergetics with trends to abnormally enhanced mitochondrial respiration that, accompanied by decreased CI, may account for the increased oxidative stress. In galactose, PRKN-PD fibroblasts exhibited decreased basal/maximal respiration vs. controls and reduced mitochondrial CIV and oxidative stress compared to glucose, suggesting an inefficient mitochondrial oxidative capacity to meet an extra metabolic requirement. PRKN-PD fibroblasts presented decreased autophagic flux with reduction of autophagy substrate and autophagosome synthesis in both conditions.The alterations exhibited under neuron-like oxidative environment (galactose), may be relevant to the disease pathogenesis potentially explaining the increased susceptibility of dopaminergic neurons to undergo degeneration. Abnormal PRKN-PD phenotype supports the usefulness of fibroblasts to model disease and the view of PD as a systemic disease where molecular alterations are present in peripheral tissues.
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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.