ReviewNeurotoxicity research2026
Decoding the RNA Shield: HNRNPC and YTHDF2 Act as Guardians of Neurons in Parkinson's Disease.
Review in Neurotoxicity research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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2 authors.
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Abstract
Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by the selective loss of dopaminergic neurons in the substantia nigra, resulting in hallmark motor symptoms such as tremor, bradykinesia, rigidity, and postural instability. Beyond these classical features, emerging evidence highlights the critical role of RNA modifications, particularly N6-methyladenosine (m6A), in regulating neuronal health and disease. The m6A modification is dynamically controlled by writers (METTL3, METTL14, WTAP), erasers (FTO, ALKBH5), and readers (e.g., YTHDF2, HNRNPC), which together influence RNA splicing, stability, and translation. Dysregulation of the readers HNRNPC and YTHDF2 has been implicated in oxidative stress, neuroinflammation, and dopaminergic neurodegeneration, positioning the HNRNPC/YTHDF2 axis as a central regulator of RNA metabolism and as a potential therapeutic target. In the healthy brain, HNRNPC ensures proper splicing and stabilizes transcripts essential for neuronal function, while YTHDF2 promotes the degeneration of deleterious m6A-modified RNAs to maintain neuronal homeostasis. In PD, their downregulation disrupts these processes, leading to transcript accumulation, impaired splicing, heightened neuroinflammation, oxidative stress, and apoptosis, contributing to dopaminergic neuron susceptibility and degeneration. We further highlight their role in α-synuclein regulation, dopaminergic signaling, and neuroimmune interactions, underscoring their promise as biomarkers and therapeutic targets. Finally, we discuss emerging therapeutic strategies targeting the m6A landscape, including antisense oligonucleotides (ASOs), RNA interference (RNAi), CRISPR-Cas13-based epitranscriptomic editing, and small-molecule modulators of m6A regulators. This review integrates molecular insights with therapeutic perspectives to elucidate how HNRNPC and YTHDF2 contribute to PD pathophysiology and explore novel avenues for interventions.
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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.