Evidence map›Paper›PMID 42789138›Full record

ArticleTranslational stroke research2026

Exogenous Hydrogen Sulfide Donors Suppress Neointimal Hyperplasia by Modulating Mitochondrial Dysfunction in Vascular Smooth Muscle Cells.

Yanyan He, Chenqing Li, Bing Zhang, Jia Liang, Chenming Si, Yang Liu, Yu Wang, Chi Ma, Tianxiao Li, Yingkun He

Abstract read
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In one paragraph

Article in Translational stroke research, 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

10 authors.

Yanyan HeCerebrovascular and Neurosurgery Department of Stroke Center, Henan Provincial People's Hospital (Zhengzhou University People's Hospital), Zhengzhou, 450003, China.
Chenqing LiDepartment of Neurosurgery, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Bing ZhangInternational Joint Laboratory of Cerebrovascular Disease of Henan Province, Henan Provincial Engineering Research Center for Cerebrovascular Interventional Innovation, Zhengzhou, 450003, China.
Jia LiangInternational Joint Laboratory of Cerebrovascular Disease of Henan Province, Henan Provincial Engineering Research Center for Cerebrovascular Interventional Innovation, Zhengzhou, 450003, China.
Chenming SiCerebrovascular and Neurosurgery Department of Stroke Center, Henan Provincial People's Hospital (Zhengzhou University People's Hospital), Zhengzhou, 450003, China.
Yang LiuCerebrovascular and Neurosurgery Department of Stroke Center, Henan Provincial People's Hospital (Zhengzhou University People's Hospital), Zhengzhou, 450003, China.
Yu WangCerebrovascular and Neurosurgery Department of Stroke Center, Henan Provincial People's Hospital (Zhengzhou University People's Hospital), Zhengzhou, 450003, China.
Chi MaDepartment of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, 100053, China.
Tianxiao LiCerebrovascular and Neurosurgery Department of Stroke Center, Henan Provincial People's Hospital (Zhengzhou University People's Hospital), Zhengzhou, 450003, China. dr.litianxiao@zzu.edu.cn.
Yingkun HeCerebrovascular and Neurosurgery Department of Stroke Center, Henan Provincial People's Hospital (Zhengzhou University People's Hospital), Zhengzhou, 450003, China. heyingkun@zzu.edu.cn.ORCID http://orcid.org/0000-0003-4168-8158

Funding

Capacity Building and Continuing Education Program of the National Health Commission GWJJ2023100101Henan Provincial Key Research and Development Program 241111313200Henan Provincial Medical Science and Technology Research Program SBGJ202303001Henan Provincial Youth Science Foundation 252300421604National Natural Science Foundation of China 8257072246
6 · The paper itself

Abstract

Phenotypic switching of vascular smooth muscle cells (VSMCs) from the contractile to the synthetic is a key factor driving the formation of intracranial atherosclerotic stenosis (ICAS); however, the upstream mitochondrial mechanisms underlying this process and its therapeutic implications remain poorly defined. This study aims to investigate the role and underlying molecular mechanisms of the mitochondria-targeted hydrogen sulfide (H

Indexed as

Hydrogen SulfideMitochondriaMuscle, Smooth, VascularMyocytes, Smooth MuscleNeointimaAnimalsHyperplasiaMaleMiceMice, Inbred C57BLOrganophosphorus CompoundsReactive Oxygen SpeciesThionesAP39 compoundHydrogen SulfideOrganophosphorus CompoundsReactive Oxygen SpeciesThionesAP39Mitochondrial DysfunctionNeointima HyperplasiaPhenotypic SwitchingVascular Smooth Muscle Cells

Identifiers

PMID42789138

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.