Evidence map›Paper›PMID 40953307›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Deficiency of SCAMP5 Triggers Pancreatic β-Cell Secretory Dysfunction and Apoptosis.

Yingqi Zhang, Donglan Tang, Chenxi Yang, Chao Lin, Yingyue Yuan, Meiying He, Yiying Chen, Zhuo Mao, Ying Ying, Xiaosong Ma and 1 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Deficiency of SCAMP5 Triggers Pancreatic β-Cell Secretory Dysfunction and Apoptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
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

11 authors.

Yingqi ZhangShenzhen University Diabetes Institute, Shenzhen Key Laboratory of Metabolism and Cardiovascular Homeostasis, Shenzhen University Medical School, Shenzhen, 518060, China.
Donglan TangShenzhen University Diabetes Institute, Shenzhen Key Laboratory of Metabolism and Cardiovascular Homeostasis, Shenzhen University Medical School, Shenzhen, 518060, China.
Chenxi YangShenzhen University Diabetes Institute, Shenzhen Key Laboratory of Metabolism and Cardiovascular Homeostasis, Shenzhen University Medical School, Shenzhen, 518060, China.
Chao LinShenzhen University Diabetes Institute, Shenzhen Key Laboratory of Metabolism and Cardiovascular Homeostasis, Shenzhen University Medical School, Shenzhen, 518060, China.
Yingyue YuanShenzhen University Diabetes Institute, Shenzhen Key Laboratory of Metabolism and Cardiovascular Homeostasis, Shenzhen University Medical School, Shenzhen, 518060, China.
Meiying HeShenzhen University Diabetes Institute, Shenzhen Key Laboratory of Metabolism and Cardiovascular Homeostasis, Shenzhen University Medical School, Shenzhen, 518060, China.
Yiying ChenShenzhen University Diabetes Institute, Shenzhen Key Laboratory of Metabolism and Cardiovascular Homeostasis, Shenzhen University Medical School, Shenzhen, 518060, China.
Zhuo MaoShenzhen University Diabetes Institute, Shenzhen Key Laboratory of Metabolism and Cardiovascular Homeostasis, Shenzhen University Medical School, Shenzhen, 518060, China.
Ying YingShenzhen University Diabetes Institute, Shenzhen Key Laboratory of Metabolism and Cardiovascular Homeostasis, Shenzhen University Medical School, Shenzhen, 518060, China.
Xiaosong MaShenzhen University Diabetes Institute, Shenzhen Key Laboratory of Metabolism and Cardiovascular Homeostasis, Shenzhen University Medical School, Shenzhen, 518060, China.
Xiangchen KongShenzhen University Diabetes Institute, Shenzhen Key Laboratory of Metabolism and Cardiovascular Homeostasis, Shenzhen University Medical School, Shenzhen, 518060, China.ORCID https://orcid.org/0000-0001-5149-1987

Funding

National Natural Science Foundation of China 82070806National Natural Science Foundation of China 82070845National Natural Science Foundation of China 82370833Natural Science Foundation of Guangdong Province 2023A1515010442Natural Science Foundation of Guangdong Province 2023A1515012688Shenzhen Key Laboratory of Metabolism and Cardiovascular Homeostasis ZDSYS20190902092903237Undergraduate innovation program of Shenzhen University S202510590101
6 · The paper itself

Abstract

The late stage of type 2 diabetes is characterized by secretory dysfunction and increased β-cell apoptosis, but the underlying mechanisms are not fully understood. The expression and function of secretory carrier membrane protein 5 (SCAMP5) in β-cells are unclear. The aim is to explore the role of SCAMP5 in diabetic β-cell failure. SCAMP5 expression is reduced in β-cells under diabetic conditions. Notably, SCAMP5 deficiency diminishes insulin secretion, which is involved in reduced Ca

Indexed as

ApoptosisDiabetes Mellitus, Type 2Insulin-Secreting CellsMembrane ProteinsAnimalsHumansInsulin SecretionMaleMiceMice, Inbred C57BLMitochondriaVoltage-Dependent Anion Channel 1Membrane ProteinsVoltage-Dependent Anion Channel 1ChREBPinsulin secretionSCAMP5VDAC1β‐cell apoptosis

Identifiers

PMID40953307
PMCPMC12677586

What OpenQuestion holds

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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.