Evidence map›Paper›PMID 39858542›Full record

ReviewBiomolecules2025

Targeting the Interplay Between Autophagy and the Nrf2 Pathway in Parkinson's Disease with Potential Therapeutic Implications.

Mengru Liu, Siqi Liu, Zihan Lin, Xi Chen, Qian Jiao, Xixun Du, Hong Jiang

Abstract readReview
In one paragraph

Review in Biomolecules, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
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

20 citing papers in PubMed.

  1. Article
  2. Ethanolic Extract ofAntioxidants (Basel, Switzerland) · 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

7 authors.

Mengru LiuDepartment of Physiology, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders and State Key Disciplines: Physiology, School of Basic Medicine, Qingdao University, Qingdao 266000, China.
Siqi LiuDepartment of Physiology, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders and State Key Disciplines: Physiology, School of Basic Medicine, Qingdao University, Qingdao 266000, China.
Zihan LinDepartment of Physiology, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders and State Key Disciplines: Physiology, School of Basic Medicine, Qingdao University, Qingdao 266000, China.
Xi ChenDepartment of Physiology, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders and State Key Disciplines: Physiology, School of Basic Medicine, Qingdao University, Qingdao 266000, China.
Qian JiaoDepartment of Physiology, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders and State Key Disciplines: Physiology, School of Basic Medicine, Qingdao University, Qingdao 266000, China.
Xixun DuDepartment of Physiology, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders and State Key Disciplines: Physiology, School of Basic Medicine, Qingdao University, Qingdao 266000, China.
Hong JiangQingdao Key Laboratory of Neurorehabilitation, Qingdao Hospital, University of Health and Rehabilitation Sciences, Qingdao 266113, China.ORCID 0000-0003-1524-7519

Funding

China Postdoctoral Science Foundation 2022M721754National Natural Science Foundation of China 32171131National Natural Science Foundation of China 32371013Natural Science Foundation of Shandong Province 2021ZDSYS11Natural Science Foundation of Shandong Province ZR2019ZD31Natural Science Foundation of Shandong Province ZR2024QH180Qingdao Postdoctoral Science Foundation QDBSH20220201054Shandong Province Postdoctoral Science Foundation SDBX2022021
6 · The paper itself

Abstract

Parkinson's disease (PD) is a prevalent neurodegenerative disorder marked by the progressive degeneration of midbrain dopaminergic neurons and resultant locomotor dysfunction. Despite over two centuries of recognition as a chronic disease, the exact pathogenesis of PD remains elusive. The onset and progression of PD involve multiple complex pathological processes, with dysfunctional autophagy and elevated oxidative stress serving as critical contributors. Notably, emerging research has underscored the interplay between autophagy and oxidative stress in PD pathogenesis. Given the limited efficacy of therapies targeting either autophagy dysfunction or oxidative stress, it is crucial to elucidate the intricate mechanisms governing their interplay in PD to develop more effective therapeutics. This review overviews the role of autophagy and nuclear factor erythroid 2-related factor 2 (Nrf2), a pivotal transcriptional regulator orchestrating cellular defense mechanisms against oxidative stress, and the complex interplay between these processes. By elucidating the intricate interplay between these key pathological processes in PD, this review will deepen our comprehensive understanding of the multifaceted pathological processes underlying PD and may uncover potential strategies for its prevention and treatment.

Indexed as

AutophagyNF-E2-Related Factor 2Parkinson DiseaseAnimalsHumansOxidative StressSignal TransductionNFE2L2 protein, humanNF-E2-Related Factor 2autophagyNrf2 pathwayoxidative stressp62Parkinson’s disease

Identifiers

PMID39858542
PMCPMC11764135

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.