Evidence map›Paper›PMID 42558147›Full record

ArticleFrontiers in pharmacology2026

Mechanistic investigation of Midkine-Notch2 signaling in suppressing pulmonary artery smooth muscle cell apoptosis and promoting vascular remodeling in hypoxic pulmonary hypertension.

Houfan Zhu, Binglong Li, Xunkai Wang, Lin Huang, Jin Peng, Jiangpeng Wu, Yong Liao, Shengchao Wei, Shijie Zhong, Guiyun Jin and 1 more

Abstract read
PubMed Full text at PMC Publisher
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Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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

11 authors.

Houfan Zhu *Key Laboratory of Emergency and Trauma of Ministry of Education, Department of Interventional Radiology and Vascular Surgery, The First Affiliated Hospital of Hainan Medical University, Hainan Medical University, Haikou, China.
Binglong Li *Key Laboratory of Emergency and Trauma of Ministry of Education, Department of Interventional Radiology and Vascular Surgery, The First Affiliated Hospital of Hainan Medical University, Hainan Medical University, Haikou, China.
Xunkai Wang *Key Laboratory of Emergency and Trauma of Ministry of Education, Department of Interventional Radiology and Vascular Surgery, The First Affiliated Hospital of Hainan Medical University, Hainan Medical University, Haikou, China.
Lin HuangDivision of Vascular Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Jin PengDepartment of Radiology, Hainan Modern Women and Children's Hospital, Haikou, China.
Jiangpeng WuKey Laboratory of Emergency and Trauma of Ministry of Education, Department of Interventional Radiology and Vascular Surgery, The First Affiliated Hospital of Hainan Medical University, Hainan Medical University, Haikou, China.
Yong LiaoKey Laboratory of Emergency and Trauma of Ministry of Education, Department of Interventional Radiology and Vascular Surgery, The First Affiliated Hospital of Hainan Medical University, Hainan Medical University, Haikou, China.
Shengchao WeiKey Laboratory of Emergency and Trauma of Ministry of Education, Department of Interventional Radiology and Vascular Surgery, The First Affiliated Hospital of Hainan Medical University, Hainan Medical University, Haikou, China.
Shijie ZhongKey Laboratory of Emergency and Trauma of Ministry of Education, Department of Interventional Radiology and Vascular Surgery, The First Affiliated Hospital of Hainan Medical University, Hainan Medical University, Haikou, China.
Guiyun JinKey Laboratory of Emergency and Trauma of Ministry of Education, Department of Interventional Radiology and Vascular Surgery, The First Affiliated Hospital of Hainan Medical University, Hainan Medical University, Haikou, China.
Tang DengKey Laboratory of Emergency and Trauma of Ministry of Education, Department of Interventional Radiology and Vascular Surgery, The First Affiliated Hospital of Hainan Medical University, Hainan Medical University, Haikou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Hypoxic pulmonary hypertension (HPH), a severe complication of chronic obstructive pulmonary disease, features pulmonary vascular remodeling driven by dysregulated pulmonary arterial smooth muscle cell (PASMC) apoptosis, with limited therapies like vasodilators offering only modest hemodynamic benefits. This study aimed to elucidate the role of Midkine (MK) in regulating PASMC apoptosis via the Notch2 pathway and its potential as a novel anti-remodeling target in HPH progression. Methods: The experimental approach involved cellular and animal models. Results: Conclusion: Unlike current vasodilators, MK drives HPH pathogenesis by suppressing PASMC apoptosis via Notch2 and exacerbating oxidative stress. Targeting MK offers a promising therapeutic strategy for HPH.

Indexed as

apoptosishypoxic pulmonary hypertension (HPH)MidkineNotch2 signaling pathwaypulmonary vascular remodeling

Identifiers

PMID42558147
PMCPMC13437302

What Socratic holds

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Registered trials

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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 Socratic graph.