Evidence map›Paper›PMID 38750218›Full record

ArticleHypertension research : official journal of the Japanese Society of Hypertension2024

Dynamin-related protein 1 mediates the therapeutic effect of isoliquiritigenin in diabetic intimal hyperplasia via regulation of mitochondrial fission.

Bao-Fu Zhang, Zi-Heng Wu, Kui Chen, Hao-Jie Jin, Jun Wu, Zi-Yi Huang, Xin-Wu Lu, Xiang-Tao Zheng

Abstract read
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Article in Hypertension research : official journal of the Japanese Society of Hypertension, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

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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

3 citing papers in PubMed.

  1. Recent advances and emerging perspectives in vascular and cardiovascular research: A 2025 update.Hypertension research : official journal of the Japanese Society of Hypertension · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Bao-Fu Zhang *Department of Vascular Surgery, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325015, China.
Zi-Heng Wu *Department of Vascular Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310003, China.
Kui Chen *Department of Vascular Surgery, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325015, China.
Hao-Jie JinDepartment of Vascular Surgery, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325015, China.
Jun WuDepartment of Vascular Surgery, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325015, China.
Zi-Yi HuangDepartment of Vascular Surgery, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325015, China.
Xin-Wu LuDepartment of Vascular Surgery, Shanghai Ninth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, China.
Xiang-Tao ZhengDepartment of Vascular Surgery, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325015, China. vaszhengxiangtao@126.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phenotypic shift of vascular smooth muscle cells (VSMCs) plays a key role in intimal hyperplasia, especially in patients with diabetes mellitus (DM). This study aimed to investigate the role of dynamin-related protein 1 (DRP1) in mitochondrial fission-mediated VSMC phenotypic shift and to clarify whether DRP1 is the therapeutic target of isoliquiritigenin (ISL). Wire injury of carotid artery or platelet-derived growth factor treatment was performed in DM mice or high-glucose cultured human aortic smooth muscle cells (HASMCs), respectively. The effects of DRP1 silencing on DM-induced intimal hyperplasia were investigated both in vivo and in vitro. Phenotypic shift of HASMCs was evaluated by detection of reactive oxygen species (ROS) generation, cell viability, and related protein expressions. The effects of ISL on DM-induced intimal hyperplasia were evaluated both in vivo and in vitro. DRP1 silencing and ISL treatment attenuated DM-induced intimal hyperplasia with reduced ROS generation, cell viability, and VSMC dedifferentiation. The GTPase domain of DRP1 protein played a critical role in mitochondrial fission in DM-induced VSMC phenotypic shift. Cellular experiments showed that ISL inhibited mitochondrial fission and reduced the GTPase activity of DRP1, which was achieved by the directly binding to K216 of the DRP1 GTPase domain. ISL attenuated mouse intimal hyperplasia by reducing GTPase activity of DRP1 and inhibiting mitochondrial fission in vivo. In conclusion, increased GTPase activity of DRP1 aggregated DM-induced intimal hyperplasia by increasing mitochondrial fission-mediated VSMC phenotypic shift. ISL attenuated mouse intimal hyperplasia by reducing DRP1 GTPase activity and inhibiting mitochondrial fission of VSMCs.

Indexed as

ChalconesDynaminsHyperplasiaMitochondrial DynamicsAnimalsCells, CulturedDiabetes Mellitus, ExperimentalHumansMaleMiceMice, Inbred C57BLMuscle, Smooth, VascularMyocytes, Smooth MuscleReactive Oxygen SpeciesTunica IntimaChalconesDnm1l protein, mouseDynaminsisoliquiritigeninReactive Oxygen SpeciesDynamin-related protein 1GTPaseIntimal hyperplasiaMitochondrial fissionVascular smooth muscle cells

Identifiers

PMID38750218

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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.