Evidence map›Paper›PMID 42432297›Full record

ArticleCardiovascular toxicology2026

SETD2 Improves Endothelial Function and Angiogenesis in Diabetic Hindlimb Ischemia Via Activating ANGPT2-PI3K/AKT Pathway.

Langtao Wang, Qing Wang, Jiaxing Duan, Yu Tan, Yuanyuan Liu, Shuai Hu, Cheng Wang, Chen Yang, Yanzhu Long, Jinxuan Wang and 6 more

Abstract read
PubMed Publisher
In one paragraph

Article in Cardiovascular toxicology, 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

16 authors.

Langtao Wang *Key Laboratory of Target Discovery and Protein Drug Development for Major Diseases (Universities), Sichuan Provincial Department of Education, School of Bioscience and Technology, Chengdu Medical College, Chengdu, 610500, China.
Qing Wang *Key Laboratory of Target Discovery and Protein Drug Development for Major Diseases (Universities), Sichuan Provincial Department of Education, School of Bioscience and Technology, Chengdu Medical College, Chengdu, 610500, China.
Jiaxing Duan *Key Laboratory of Target Discovery and Protein Drug Development for Major Diseases (Universities), Sichuan Provincial Department of Education, School of Bioscience and Technology, Chengdu Medical College, Chengdu, 610500, China.
Yu TanAging Mechanisms and Interventions Key Laboratory of Sichuan Province, School of Basic Medical Sciences, Chengdu Medical College, Chengdu, 610500, China.
Yuanyuan LiuAging Mechanisms and Interventions Key Laboratory of Sichuan Province, School of Basic Medical Sciences, Chengdu Medical College, Chengdu, 610500, China.
Shuai HuKey Laboratory of Target Discovery and Protein Drug Development for Major Diseases (Universities), Sichuan Provincial Department of Education, School of Bioscience and Technology, Chengdu Medical College, Chengdu, 610500, China.
Cheng WangKey Laboratory of Target Discovery and Protein Drug Development for Major Diseases (Universities), Sichuan Provincial Department of Education, School of Bioscience and Technology, Chengdu Medical College, Chengdu, 610500, China.
Chen YangKey Laboratory of Target Discovery and Protein Drug Development for Major Diseases (Universities), Sichuan Provincial Department of Education, School of Bioscience and Technology, Chengdu Medical College, Chengdu, 610500, China.
Yanzhu LongKey Laboratory of Target Discovery and Protein Drug Development for Major Diseases (Universities), Sichuan Provincial Department of Education, School of Bioscience and Technology, Chengdu Medical College, Chengdu, 610500, China.
Jinxuan WangAging Mechanisms and Interventions Key Laboratory of Sichuan Province, School of Basic Medical Sciences, Chengdu Medical College, Chengdu, 610500, China.
Tao YuKey Laboratory of Target Discovery and Protein Drug Development for Major Diseases (Universities), Sichuan Provincial Department of Education, School of Bioscience and Technology, Chengdu Medical College, Chengdu, 610500, China.
Tianhu LiuCardiology and Vascular Health Research Center, Chengdu Medical College, Chengdu, 611730, Sichuan, China.
Yaping LanCardiology and Vascular Health Research Center, Chengdu Medical College, Chengdu, 611730, Sichuan, China.
Chaoping YuCardiology and Vascular Health Research Center, Chengdu Medical College, Chengdu, 611730, Sichuan, China. 53260837@qq.com.
Liping LuoKey Laboratory of Target Discovery and Protein Drug Development for Major Diseases (Universities), Sichuan Provincial Department of Education, School of Bioscience and Technology, Chengdu Medical College, Chengdu, 610500, China. 102023003@cmc.edu.cn.
Xiaozhen DaiKey Laboratory of Target Discovery and Protein Drug Development for Major Diseases (Universities), Sichuan Provincial Department of Education, School of Bioscience and Technology, Chengdu Medical College, Chengdu, 610500, China. daixiaozhen@cmc.edu.cn.

Funding

Chengdu Medical College Third Affiliated Hospital 23LHPDZYB19Chengdu Medical College Third Affiliated Hospital 23LHPDZZD03Chengdu Municipal Health Commission 2021432Sichuan Science and Technology Education Joint Foundation 2024NSFSC2088The Chengdu Medical University Science and Technology Innovation Team 2024kjTzn07the National Key Technology R & D Program of China 2023YFB3810100the National Natural Science Foundation of China 82400488the National Natural Science Foundation of China 82470485the Organized Research Initiatives of Chengdu Medical College CYYZZ25-06the Sichuan Provincial Administration of Traditional Chinese Medicine 2024zd028
6 · The paper itself

Abstract

Vascular endothelial dysfunction serves as a key pathological basis for diabetic vascular complications. Enhancing endothelial function and promoting angiogenesis are therefore critical strategies in the treatment of diabetic lower hindlimb ischemia (HLI). SETD2 is the primary methyltransferase for H3K36 trimethylation (H3K36me3) and is involved in vascular development, but its role in diabetes-associated endothelial dysfunction remains unknown. This study aimed to investigate the function and underlying mechanism of SETD2 in endothelial cells under diabetic conditions and in the context of diabetic HLI. A diabetic mouse model was established in endothelial-specific conditional SETD2 knockout (SETD2

Indexed as

Angiopoietin-2Diabetes Mellitus, ExperimentalDiabetic AngiopathiesHistone-Lysine N-MethyltransferaseHuman Umbilical Vein Endothelial CellsIschemiaMuscle, SkeletalNeovascularization, PhysiologicPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktAnimalsCell MovementCell ProliferationCells, CulturedHindlimbHumansAngiopoietin-2Angpt2 protein, mouseHistone-Lysine N-MethyltransferasePhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktSETD2 protein, mouseAngiogenesisANGPT2Diabetes mellitusEndothelial cellsHindlimb ischemiaSETD2

Identifiers

PMID42432297

What Socratic holds

Textmetadata
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.