ArticleCell death & disease2018
Defective mitochondrial protein import contributes to complex I-induced mitochondrial dysfunction and neurodegeneration in Parkinson's disease.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
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Who cites it
75 citing papers in PubMed, 146 citations in OpenAlex.
- Proteostasis of organelles in aging and disease.The FEBS journal · 2026Review
- Selective vulnerability of dopaminergic neurons in Parkinson's disease connects PRKN and differential expression of CHCHD2 and GPNMB.Cell death & disease · 2026Article
- Targeting prohibitins activates the ISR through DELE1-HRI by impairing protein import into the mitochondrial matrix.Cell death and differentiation · 2026Article
- Mitochondrial CircRNA CircMT-RNR2 Safeguards Antioxidant Defense to Support Fibroblast Functions in Wound Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Roles of mitophagy and immune infiltration in Parkinson's disease: new perspectives from bioinformatics analysis and A53T transgenic mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- The genetic associations of DNAJC family members with Parkinson's disease: comprehensive evidence from burden analysis and Mendelian randomization.Human genetics · 2026Article
- The role of TOMM20 in Mediating TERT translocation to mitochondria and its impact on mitophagy in membranous nephropathy.BMC nephrology · 2026Article
- Early mitophagy activation by Urolithin A prevents, but late activation does not reverse, age-related cognitive impairment.npj aging · 2026Article
- Multi-Omics Analysis Reveals Distinct Lipid Remodelling and Mitochondrial Stress in SH-SY5Y Cells Modelling Parkinson's Disease.Metabolites · 2025Article
- SENP6 Maintains Mitochondrial Homeostasis by Regulating Mitochondrial Protein Import Through deSUMOylation of TOM40.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- Mitochondrial protein import stress augments α-synuclein aggregation and neural damage independent of bioenergetics.Research square · 2025Article
- COVID-19 Alters Inflammatory, Mitochondrial, and Protein Clearance Pathway Genes: Potential Implications for New-onset Parkinsonism in Patients.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- DNA damage response regulator ATR licenses PINK1-mediated mitophagy.Nucleic acids research · 2025Article
- Evaluation of Mitochondrial Phagy (Mitophagy) in Human Non-small Adenocarcinoma Tumor Cells.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Alpha-Mangostin Alleviates Mitochondrial Damage and Autophagy Dysregulation in the MPPAdvances in pharmacological and pharmaceutical sciences · 2025Article
- LETMD1 regulates mitochondrial protein synthesis and import to guard brown fat mitochondrial integrity and function.iScience · 2024Article
- The Role and Mechanism of Ambra1-Mediated Mitophagy in TDCPP-Exposed Mouse Hippocampal Neurons.Neurochemical research · 2024Article
- The E3 ligase HUWE1 increases the sensitivity of CRC to oxaliplatin through TOMM20 degradation.Oncogene · 2024Article
- Mitochondrial damage and impaired mitophagy contribute to disease progression in SCA6.Acta neuropathologica · 2024Article
15 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Mitochondria are the prime energy source in most eukaryotic cells, but these highly dynamic organelles are also involved in a multitude of cellular events. Disruption of mitochondrial homeostasis and the subsequent mitochondrial dysfunction plays a key role in the pathophysiology of Parkinson's disease (PD). Therefore, maintenance of mitochondrial integrity through different surveillance mechanisms is critical for neuronal survival. Here, we have studied the mitochondrial protein import system in in vitro and in vivo models of PD. Complex I inhibition, a characteristic pathological hallmark in PD, impaired mitochondrial protein import, which was associated with a downregulation of two key components of the system: translocase of the outer membrane 20 (TOM20) and translocase of the inner membrane 23 (TIM23), both in vitro and in vivo. In vitro, those changes were associated with OXPHOS protein downregulation, accumulation of aggregated proteins inside mitochondria and downregulation of mitochondrial chaperones. Most of these pathogenic changes, including mitochondrial dysfunction and dopaminergic cell death, were abrogated by TOM20 or TIM23 overexpression, in vitro. However, in vivo, while TOM20 overexpression exacerbated neurodegeneration in both substantia nigra (SN) pars compacta (pc) and striatum, overexpression of TIM23 partially protected dopaminergic neurons in the SNpc. These results highlight mitochondrial protein import dysfunction and the distinct role of two of their components in the pathogenesis of PD and suggest the need for future studies to further characterize mitochondrial protein import deficit in the context of PD.
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