Evidence map›Paper›PMID 40170616›Full record

ArticleActa biochimica et biophysica Sinica2025

TLR4 mediates lipotoxic β-cell dysfunction by inhibiting the TMEM24/PI3K/AKT pathway.

Chao Lan, Yan Li, Zhiyan Weng, Wei Pan, Wanxin Lin, Zhen Jiang, Liyong Yang, Ximei Shen

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta biochimica et biophysica Sinica, 2025. 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

8 authors.

Chao LanDepartment of Endocrinology, the First Affiliated Hospital, Fujian Medical University, Fuzhou 350005, China.
Yan LiDepartment of Endocrinology, the First Affiliated Hospital, Fujian Medical University, Fuzhou 350005, China.
Zhiyan WengDepartment of Endocrinology, the First Affiliated Hospital, Fujian Medical University, Fuzhou 350005, China.
Wei PanDepartment of Endocrinology, the First Affiliated Hospital, Fujian Medical University, Fuzhou 350005, China.
Wanxin LinDepartment of Endocrinology, the First Affiliated Hospital, Fujian Medical University, Fuzhou 350005, China.
Zhen JiangDepartment of Endocrinology, the First Affiliated Hospital, Fujian Medical University, Fuzhou 350005, China.
Liyong YangDepartment of Endocrinology, the First Affiliated Hospital, Fujian Medical University, Fuzhou 350005, China.
Ximei ShenDepartment of Endocrinology, the First Affiliated Hospital, Fujian Medical University, Fuzhou 350005, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune imbalance is the core pathophysiological mechanism of the deterioration of β-cell function driven by lipid metabolism disorders. Toll-like receptor 4 (TLR4) inflammatory signaling is a key pathway that mediates lipotoxic injury in β-cells, but the underlying mechanism needs to be further elucidated. Transmembrane protein 24 (TMEM24) is a key transporter that regulates pulsatile insulin secretion, but its pathophysiology in lipotoxicity remains unclear. In this study, we investigate whether TLR4-mediated lipotoxicity is affected by the inhibition of TMEM24 expression. The PPI network shows that TLR4 is associated with both insulin secretion and ER stress proteins in islets from obese rats. Using

Indexed as

Insulin-Secreting CellsMembrane ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionToll-Like Receptor 4AnimalsInsulinMaleObesityPalmitic AcidRatsRats, Sprague-DawleyInsulinMembrane ProteinsPalmitic AcidPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTlr4 protein, ratToll-Like Receptor 4lipotoxicitymetabolic inflammationTLR4TMEM24β-cell function

Identifiers

PMID40170616
PMCPMC12616714

What OpenQuestion holds

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Registered trials

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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 OpenQuestion graph.