ReviewFrontiers in neurology2025
The metabolic-epigenetic interface: lysine succinylation orchestrates bidirectional crosstalk in neurodegenerative disorders.
Review in Frontiers in neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Post-translational modifications as a regulatory code for tau function in health and disease.Frontiers in dementia · 2026Review
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Authors and funding
4 authors.
Funding
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Abstract
Succinylation, a nexus between metabolism and epigenetic regulation, is a central factor in the onset and progression of neurodegenerative diseases (NDDs). Research has demonstrated a close association between NDDs and neuronal metabolic disorders. Succinylation regulates the interaction between energy metabolism and epigenetic networks, establishing the pathological mechanism of "metabolic-epigenetic bidirectional regulation." In metabolic stress, such as mitochondrial dysfunction or enhanced glycolysis, succinyl-CoA increases, causing uncontrolled succinylation. These modifications impair the function of proteins associated with synaptic plasticity, leading to disorders in synaptic transmission and neuronal damage. Concurrently, succinylation regulates the activity of enzymes involved in DNA methylation and epigenetic reprogramming, impairing neuronal recovery and creating a vicious cycle. This regulatory network displays bidirectional self-reinforcing characteristics. Metabolic disorders influence epigenetic states through succinylation. Epigenetic abnormalities inhibit the transcription of genes associated with mitochondrial metabolism, exacerbating energy metabolism defects and oxidative stress. This leads to irreversible degenerative changes in neurons. At the therapeutic level, targeting succinylation can disrupt the metabolic-epigenetic pathological loop and restore synaptic function. In short, understanding how succinylation is regulated may lead to new treatment options for neurodegenerative diseases.
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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 Socratic graph.