Evidence map›Paper›PMID 38409852›Full record

ArticleAutophagy2024

Sodium butyrate ameliorates high glucose-suppressed neuronal mitophagy by restoring PRKN expression via inhibiting the RELA-HDAC8 complex.

Ji Hyeon Cho, Chang Woo Chae, Jae Ryong Lim, Young Hyun Jung, Su Jong Han, Jee Hyeon Yoon, Ji Yong Park, Ho Jae Han

Open access · greenAbstract read
In one paragraph

Article in Autophagy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
9.7field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 25 citations in OpenAlex.

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  4. The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Ji Hyeon ChoDepartment of Veterinary Physiology, College of Veterinary Medicine, Research Institute for Veterinary Science, and BK21 FOUR Future Veterinary Medicine Leading Education & Research Center, Seoul National University, Seoul, South Korea.
Chang Woo ChaeDepartment of Veterinary Physiology, College of Veterinary Medicine, Research Institute for Veterinary Science, and BK21 FOUR Future Veterinary Medicine Leading Education & Research Center, Seoul National University, Seoul, South Korea.
Jae Ryong LimDepartment of Veterinary Physiology, College of Veterinary Medicine, Research Institute for Veterinary Science, and BK21 FOUR Future Veterinary Medicine Leading Education & Research Center, Seoul National University, Seoul, South Korea.
Young Hyun JungDepartment of Veterinary Physiology, College of Veterinary Medicine, Research Institute for Veterinary Science, and BK21 FOUR Future Veterinary Medicine Leading Education & Research Center, Seoul National University, Seoul, South Korea.
Su Jong HanDepartment of Veterinary Physiology, College of Veterinary Medicine, Research Institute for Veterinary Science, and BK21 FOUR Future Veterinary Medicine Leading Education & Research Center, Seoul National University, Seoul, South Korea.
Jee Hyeon YoonDepartment of Veterinary Physiology, College of Veterinary Medicine, Research Institute for Veterinary Science, and BK21 FOUR Future Veterinary Medicine Leading Education & Research Center, Seoul National University, Seoul, South Korea.
Ji Yong ParkDepartment of Veterinary Physiology, College of Veterinary Medicine, Research Institute for Veterinary Science, and BK21 FOUR Future Veterinary Medicine Leading Education & Research Center, Seoul National University, Seoul, South Korea.
Ho Jae HanDepartment of Veterinary Physiology, College of Veterinary Medicine, Research Institute for Veterinary Science, and BK21 FOUR Future Veterinary Medicine Leading Education & Research Center, Seoul National University, Seoul, South Korea.
Seoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Damaged mitochondria accumulation in diabetes is one of the main features that contribute to increased incidence of cognitive impairment by inducing apoptosis. Butyrate is a major metabolite produced by microbiota that has neuroprotective effects by regulating mitochondrial function. However, detailed mechanisms underlying how butyrate can regulate neuronal mitophagy remain unclear. Here, we examined the regulatory effects of sodium butyrate (NaB) on high glucose-induced mitophagy dysregulation, neuronal apoptosis, and cognitive impairment and its underlying mechanisms in human-induced pluripotent stem cell-derived neurons, SH-SY5Ys, and streptozotocin (STZ)-induced diabetic mice. In our results, diabetic mice showed gut-microbiota dysbiosis, especially a decreased number of butyrate-producing bacteria and reduced NaB plasma concentration. NaB ameliorated high glucose-induced neuronal mitochondrial dysfunction by recovering PRKN/Parkin-mediated mitophagy. High glucose-induced reactive oxygen species (ROS) and -inhibited PRKAA/AMPKα stimulated the RELA/p65-HDAC8 complex, which downregulated PRKN protein expression by binding to the

Indexed as

Butyric AcidGlucoseHistone DeacetylasesMitophagyNeuronsTranscription Factor RelAAnimalsApoptosisDiabetes Mellitus, ExperimentalHumansInduced Pluripotent Stem CellsMaleMiceMice, Inbred C57BLMitochondriaRepressor ProteinsButyric AcidGlucoseHistone Deacetylasesparkin proteinRepressor ProteinsTranscription Factor RelAUbiquitin-Protein Ligasesautophagydiabetesgut-brain axismitochondrianeuronal apoptosisshort-chain fatty acids

Identifiers

PMID38409852
PMCPMC11210903
OpenAlexW4392194543

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.