Evidence map›Paper›PMID 41723748›Full record

ArticleIslets2026

Annexin A1 exacerbates islet stellate cell activation by regulating triglyceride catabolism via the PPARα/ACOX1/CYP4a pathway.

Qing Li, Yan Zhang, Tianpei Yu, Li Shi, Qinqin Qiu, Ben Wang, Yiquan Sang, Rui Li, Qian Lv, Jie Wang and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Islets, 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

15 authors.

Qing LiDepartment of Endocrinology, Affiliated Xuzhou Central Hospital of Southeast University, The Xuzhou Clinical College of Xuzhou Medical University, Xuzhou Clinical School of Nanjing Medical University, Xuzhou Central Hospital, Xuzhou, People's Republic of China.
Yan ZhangDepartment of Endocrinology, Affiliated Xuzhou Central Hospital of Southeast University, The Xuzhou Clinical College of Xuzhou Medical University, Xuzhou Clinical School of Nanjing Medical University, Xuzhou Central Hospital, Xuzhou, People's Republic of China.
Tianpei YuDepartment of Endocrinology, Affiliated Xuzhou Central Hospital of Southeast University, The Xuzhou Clinical College of Xuzhou Medical University, Xuzhou Clinical School of Nanjing Medical University, Xuzhou Central Hospital, Xuzhou, People's Republic of China.
Li ShiDepartment of Endocrinology, Affiliated Xuzhou Central Hospital of Southeast University, The Xuzhou Clinical College of Xuzhou Medical University, Xuzhou Clinical School of Nanjing Medical University, Xuzhou Central Hospital, Xuzhou, People's Republic of China.
Qinqin QiuDepartment of Endocrinology, Affiliated Xuzhou Central Hospital of Southeast University, The Xuzhou Clinical College of Xuzhou Medical University, Xuzhou Clinical School of Nanjing Medical University, Xuzhou Central Hospital, Xuzhou, People's Republic of China.
Ben WangDepartment of Endocrinology, Affiliated Xuzhou Central Hospital of Southeast University, The Xuzhou Clinical College of Xuzhou Medical University, Xuzhou Clinical School of Nanjing Medical University, Xuzhou Central Hospital, Xuzhou, People's Republic of China.
Yiquan SangDepartment of Endocrinology, Affiliated Xuzhou Central Hospital of Southeast University, The Xuzhou Clinical College of Xuzhou Medical University, Xuzhou Clinical School of Nanjing Medical University, Xuzhou Central Hospital, Xuzhou, People's Republic of China.
Rui LiDepartment of Endocrinology, Affiliated Xuzhou Central Hospital of Southeast University, The Xuzhou Clinical College of Xuzhou Medical University, Xuzhou Clinical School of Nanjing Medical University, Xuzhou Central Hospital, Xuzhou, People's Republic of China.
Qian LvDepartment of Endocrinology, Affiliated Xuzhou Central Hospital of Southeast University, The Xuzhou Clinical College of Xuzhou Medical University, Xuzhou Clinical School of Nanjing Medical University, Xuzhou Central Hospital, Xuzhou, People's Republic of China.
Jie WangDepartment of Endocrinology, Affiliated Xuzhou Central Hospital of Southeast University, The Xuzhou Clinical College of Xuzhou Medical University, Xuzhou Clinical School of Nanjing Medical University, Xuzhou Central Hospital, Xuzhou, People's Republic of China.
Xuekui LiuDepartment of Endocrinology, Affiliated Xuzhou Central Hospital of Southeast University, The Xuzhou Clinical College of Xuzhou Medical University, Xuzhou Clinical School of Nanjing Medical University, Xuzhou Central Hospital, Xuzhou, People's Republic of China.
Houfa GengDepartment of Endocrinology, Affiliated Xuzhou Central Hospital of Southeast University, The Xuzhou Clinical College of Xuzhou Medical University, Xuzhou Clinical School of Nanjing Medical University, Xuzhou Central Hospital, Xuzhou, People's Republic of China.
Peter M JonesDiabetes & Obesity, School of Cardiovascular and Metabolic Medicine & Sciences, King's College London, London, UK.
Jun LiangDepartment of Endocrinology, Affiliated Xuzhou Central Hospital of Southeast University, The Xuzhou Clinical College of Xuzhou Medical University, Xuzhou Clinical School of Nanjing Medical University, Xuzhou Central Hospital, Xuzhou, People's Republic of China.
Wei XuDepartment of Endocrinology, Affiliated Xuzhou Central Hospital of Southeast University, The Xuzhou Clinical College of Xuzhou Medical University, Xuzhou Clinical School of Nanjing Medical University, Xuzhou Central Hospital, Xuzhou, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundActivation of islet stellate cells (ISCs) contributes to islet fibrosis and diabetes progression through excessive extracellular matrix secretion and lipid loss. Annexin A1 (ANXA1) has been reported to modulate lipid metabolism in other tissues, but its role in ISCs remains unclear.

methodsISCs were isolated from 9-and 28-week-old db/m and db/db mice. Lipid content analysis, qRT‒PCR, and Western blotting were used to assess lipid metabolism-related molecules. ANXA1 expression was analyzed by immunohistochemistry and Western blotting. Recombinant ANXA1 was co-cultured with db/db ISCs to evaluate lipid synthesis and lipolysis. The interaction between ANXA1 and peroxisome proliferator-activated receptor alpha (PPARα) was examined by immunoprecipitation.

resultsActivation of ISCs markedly reduced intracellular triglycerides, with decreased Diacylglycerol Acyltransferase 1/2 (DGAT1/2) and increased adipose triglyceride lipase (ATGL) and hormone-sensitive triglyceride lipase (HSL) expression. ANXA1 was detected in islets, MIN6 cells, and their culture supernatants. Recombinant ANXA1 treatment lowered triglyceride levels and upregulated PPARα and its downstream genes, acyl-CoA oxidase 1 (ACOX1) and cytochrome P450 4 A (CYP4A); these effects were enhanced by a PPARα agonist but reversed by inhibition. Immunofluorescence and coimmunoprecipitation confirmed that PPARα acts as a key mediator of ANXA1-regulated triglyceride metabolism in ISCs.

conclusionANXA1 promotes ISCs activation by enhancing triglyceride catabolism through the PPARα signaling pathway, suggesting a novel therapeutic target for islet fibrosis.

Indexed as

Annexin A1Islets of LangerhansPancreatic Stellate CellsPPAR alphaTriglyceridesAnimalsLipid MetabolismMaleMiceMice, Inbred C57BLSignal TransductionAnnexin A1annexin A1, mousePPAR alphaPpara protein, mouseTriglyceridesANXA1Islet fibrosisIslet stellate cellslipid metabolismPPARα

Identifiers

PMID41723748
PMCPMC12928626

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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.