Evidence map›Paper›PMID 42066513›Full record

ArticleRedox biology2026

RAB5A regulates cell proliferation and lipid metabolism by modulating mitochondrial ROS via AMPK signaling pathway in ovarian granulosa cells.

Shao-Hong Liu, Ping Yang, Bing-Hong Zhu, Hong-Yu Li, Shan Wang, Yong Wang, Xiao-Man Liu

Abstract read
In one paragraph

Article in Redox biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Shao-Hong LiuDepartment of Clinical Laboratory, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, China; Central Laboratory, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, China.
Ping YangDepartment of Obstetrics and Gynecology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, China.
Bing-Hong ZhuDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Shandong First Medical Universit, Shandong Provincial Qianfoshan Hospital, Jinan, 250014, China.
Hong-Yu LiDepartment of Reproductive Medicine, Department of Obstetrics and Gynecology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, 250021, China; Shandong Key Laboratory of Reproductive Research and Birth Defect Prevention, Shandong First Medical University, Jinan, Shandong, 250021, China; Jinan Engineering Laboratory of Reproductive Diagnosis and Treatment Technology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, 250021, China.
Shan WangDepartment of Reproductive Medicine, Department of Obstetrics and Gynecology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, 250021, China; Shandong Key Laboratory of Reproductive Research and Birth Defect Prevention, Shandong First Medical University, Jinan, Shandong, 250021, China; Jinan Engineering Laboratory of Reproductive Diagnosis and Treatment Technology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, 250021, China; Shandong Second Medical University, Weifang, Shandong, 252422, China.
Yong WangDepartment of Clinical Laboratory, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, China. Electronic address: sdwangyong@126.com.
Xiao-Man LiuCentral Laboratory, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, China. Electronic address: liuxiaoman@sdfmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ovarian granulosa cells (GCs) play a crucial role in follicle development and hormone production. These functions require substantial energy, supported by mitochondrial activity and balanced lipid metabolism. RAB5 is known to maintain mitochondrial homeostasis; however, its role in regulating lipid metabolism via the energy-sensing AMP-activated protein kinase (AMPK) pathway remains unclear. In polycystic ovary syndrome (PCOS), a disorder often linked to metabolic and mitochondrial defects in GCs, RAB5A levels are significantly reduced in obese subtypes. In this study, we demonstrate that RAB5A deficiency disrupts lipid metabolism and impairs normal cell proliferation, characterized by increased mitochondrial stress (increased reactive oxygen species) and activation of mitophagy via AMPK. RAB5A may coordinate with MIGA2, a protein involved in regulating mitochondria-lipid droplet interactions, to modulate lipid metabolism via AMPK activity. Notably, activating AMPK with AICAR reverses the adverse effects of RAB5A loss. Collectively, these findings identify RAB5A as a key regulator of GC function and a potential therapeutic target in obese PCOS.

Indexed as

AMP-Activated Protein KinasesGranulosa CellsLipid MetabolismMitochondriarab5 GTP-Binding ProteinsReactive Oxygen SpeciesAnimalsCell ProliferationFemaleHumansPolycystic Ovary SyndromeSignal TransductionAMP-Activated Protein KinasesRAB5C protein, humanrab5 GTP-Binding ProteinsReactive Oxygen SpeciesAMPKCell proliferationLipid metabolismMIGA2MitochondriaRAB5A

Identifiers

PMID42066513
PMCPMC13144571

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.