Evidence map›Paper›PMID 41444229›Full record

ArticleNature communications2025

Calcium channel blockers increase the risk of aortic aneurysm and dissection.

Tianfeng Ma, Zeyu Cai, Xinming Xu, Long Cao, Ao Wang, Zhongshuang Zhang, Siting Zhang, Zhenkun Huang, Jingjing Luo, Sen Lin and 10 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
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

20 authors.

Tianfeng Ma *Department of Vascular and Endovascular Surgery, Chinese PLA General Hospital, Beijing, China.ORCID http://orcid.org/0000-0001-7571-0996
Zeyu Cai *Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China.
Xinming Xu *Department of Nutrition and Food Hygiene, School of Public Health, Institute of Nutrition, Fudan University, Shanghai, China.
Long Cao *Department of Vascular and Endovascular Surgery, Chinese PLA General Hospital, Beijing, China.
Ao WangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China.
Zhongshuang ZhangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China.
Siting ZhangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China.
Zhenkun HuangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China.
Jingjing LuoDepartment of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Sen LinDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China.
Jiashu GeDepartment of Vascular and Endovascular Surgery, Chinese PLA General Hospital, Beijing, China.
Xinhao WangDepartment of Vascular and Endovascular Surgery, Chinese PLA General Hospital, Beijing, China.
Yi FuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China.ORCID http://orcid.org/0000-0002-8832-9331
Fang YuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China.
Jing ZhouDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China.ORCID http://orcid.org/0000-0002-2211-4901
Lixin WangDepartment of Vascular Surgery, Zhongshan Hospital, Fudan University; Vascular Surgery Institute of Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0002-1379-3906
Hongpeng ZhangDepartment of Vascular and Endovascular Surgery, Chinese PLA General Hospital, Beijing, China.
Xiang GaoDepartment of Nutrition and Food Hygiene, School of Public Health, Institute of Nutrition, Fudan University, Shanghai, China. xiang_gao@fudan.edu.cn.ORCID http://orcid.org/0000-0003-2617-6509
Wei GuoDepartment of Vascular and Endovascular Surgery, Chinese PLA General Hospital, Beijing, China. guoweiplagh@sina.com.ORCID http://orcid.org/0000-0001-6212-8390
Wei KongDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China. kongw@bjmu.edu.cn.ORCID http://orcid.org/0000-0001-6720-6810

Funding

China Postdoctoral Science Foundation 2025M771404National Natural Science Foundation of China (National Science Foundation of China) 82070494National Natural Science Foundation of China (National Science Foundation of China) 82230010National Natural Science Foundation of China (National Science Foundation of China) 82300544National Natural Science Foundation of China (National Science Foundation of China) 82473622
6 · The paper itself

Abstract

Aortic aneurysm and dissection (AAD) are life-threatening conditions without effective medications. Impaired contractility of vascular smooth muscle cells (VSMCs) is strongly linked to AAD, but the role of calcium channel blockers (CCBs), which directly inhibits VSMC contractility, in AAD remains unclear. Here we showed data from 501,878 initially AAD-free participants in UK Biobank. Over a median follow-up of 13.5 years, CCB users had higher AAD risk (HR = 1.31) than hypertensive patients not receiving antihypertensive treatment. In mouse models of AAD, CCBs significantly aggravated aortic stiffness and AAD development. For patients with type B aortic dissection who underwent endovascular repair, CCBs limited AAD regression compared with other antihypertensives. Moreover, silencing of protein kinase cGMP-dependent 1 (PRKG1) significantly mitigated CCB-aggravated AAD progression. These findings suggest that CCBs may increase AAD risk and post-stent surgery prognosis, highlighting the need for caution when prescribing CCBs to hypertensive patients at risk for AAD.

Indexed as

Aortic AneurysmAortic DissectionCalcium Channel BlockersAgedAnimalsAntihypertensive AgentsDisease Models, AnimalFemaleFollow-Up StudiesHumansHypertensionMaleMiceMiddle AgedMuscle, Smooth, VascularMyocytes, Smooth MuscleAntihypertensive AgentsCalcium Channel Blockers

Identifiers

PMID41444229
PMCPMC12873303

What OpenQuestion 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 OpenQuestion graph.