ArticleActa biochimica et biophysica Sinica2022
MTERF3 contributes to MPP+-induced mitochondrial dysfunction in SH-SY5Y cells.
Article in Acta biochimica et biophysica Sinica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 3 citations in OpenAlex.
- [CHIR99021 alleviates neuroinflammation in a mouse model of Parkinson's disease by inhibiting the GSK-3β/NF-κB pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Identification of characteristic genes ofanddeficiency constitutions: an integrated analysis based on bioinformatics and machine learning.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- Neuroprotective effects and mechanisms of the YiQiWenYangSanHan formula on Parkinson's disease mice.IBRO neuroscience reports · 2025Article
- Identification and validation of biomarkers related to mitophagy in chronic obstructive pulmonary disease.Molecular medicine reports · 2025Article
- Establishment of Risk Model and Analysis of Immunoinfiltration Based on Mitophagy-Related Associated Genes in Atrial Fibrillation.Journal of inflammation research · 2023Article
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7 authors at 1 institution in 1 country.
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Abstract
Parkinson's disease (PD) is a neurodegenerative disorder causing severe social and economic burdens. The origin of PD has been usually attributed to mitochondrial dysfunction. To this end, mitochondrial transcription regulators become attractive subjects for understanding PD pathogenesis. Previously, we found that the expression of mitochondrial transcription termination factor 3 (MTERF3) was reduced in MPP+-induced mice model of PD. In the present study, we probe the function of MTERF3 and its role in MPP+-induced cellular model of PD. Initially, we observe that MTERF3 expression is also reduced in MPP+-induced cellular model of PD, which can be mainly attributed to the increase of MTERF3 degradation. Next, we examine the effect of MTERF3 knockdown and overexpression on the replication, transcription, and translation of mitochondrial DNA (mtDNA). We show that knockdown and overexpression of MTERF3 have opposite effects on mtDNA transcript level but similar effects on mtDNA expression level, in line with MTERF3's dual roles in mtDNA transcription and translation. In addition, we examine the effect of MTERF3 knockdown and overexpression on mitochondrial function with and without MPP+ treatment, and find that MTERF3 seems to play a generally protective role in MPP+-induced mitochondrial dysfunction. Together, this work suggests a regulatory role of MTERF3 in MPP+-induced cellular model of PD and may provide clues in designing novel therapeutics against PD.
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