Evidence map›Paper›PMID 37410531›Full record

ArticlePharmaceutical biology2023

Hydroxysafflor yellow A inhibits endothelial cell ferroptosis in diabetic atherosclerosis mice by regulating miR-429/SLC7A11.

Jianjie Rong, Chuanyong Li, Qiang Zhang, Guangfeng Zheng, Weijian Fan, Zhichang Pan, Shuming Shi

Open access · goldAbstract read
In one paragraph

Article in Pharmaceutical biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
10.6field-weighted citation impact, top 1% of its field
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

33 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Ferroptosis as a target mechanism in heart and kidney disease.The Journal of clinical investigation · 2026
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  10. Mechanistic Role of Disulfidptosis in Type 2 Diabetes Mellitus.Molecular nutrition & food research · 2026
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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 at 2 institutions in 1 country.

Jianjie RongDepartment of Vascular Surgery, Suzhou TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Suzhou, P. R. China.
Chuanyong LiDepartment of Vascular Surgery, Suzhou TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Suzhou, P. R. China.
Qiang ZhangDepartment of Vascular Surgery, Suzhou TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Suzhou, P. R. China.
Guangfeng ZhengDepartment of Vascular Surgery, Suzhou TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Suzhou, P. R. China.
Weijian FanDepartment of Vascular Surgery, Suzhou TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Suzhou, P. R. China.
Zhichang PanDepartment of Vascular Surgery, Suzhou TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Suzhou, P. R. China.
Shuming ShiDepartment of Vascular Surgery, Suzhou TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Suzhou, P. R. China.
Nanjing University of Chinese Medicine · CNSuzhou Traditional Chinese Medicine Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

contextFerroptosis may play an essential role in lipid peroxidation and endothelial dysfunction of aortic endothelial cells (ECs) in type 2 diabetes mellitus (T2DM) with atherosclerosis (AS). Hydroxysafflor yellow A (HSYA) has shown substantial antioxidant stress and anti-ferroptosis.

objectiveThis study confirms whether HSYA improves symptoms in a mouse model of T2DM/AS and elucidates the underlying mechanisms. MATERIALS AND

methodsApoE

resultsHSYA effectively reduced atherosclerotic plaque formation in the T2DM/AS mouse model and inhibited HUVEC ferroptosis, such as upregulating GSH-Px, SLC7A11 and GPX4, but inhibited ACSL4. Furthermore, HSYA also downregulated the expression of miR-429, which further regulated SLC7A11 expression. After miR-429 mimic or SLC7A11 siRNA transfection in the HUVEC, the antioxidative stress and anti-ferroptosis effects of HSYA were significantly abolished.

conclusionsHSYA is expected to become an important health drug to prevent the occurrence and development of T2DM/AS.

Indexed as

AtherosclerosisDiabetes Mellitus, Type 2MicroRNAsAmino Acid Transport System y+AnimalsApolipoproteins EChalconeDisease Models, AnimalHumansHuman Umbilical Vein Endothelial CellsMiceQuinonesAmino Acid Transport System y+Apolipoproteins EChalconehydroxysafflor yellow AMicroRNAsMIRN429 microRNA, humanMIRN429 microRNA, mouseQuinonesSLC7A11 protein, humanApoE-/- miceHUVECOx-LDLType 2 diabetes mellitus with atherosclerosis

Identifiers

PMID37410531
PMCPMC10327525
OpenAlexW4383301999

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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 OpenQuestion graph.