Evidence map›Paper›PMID 41894331›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2026

CALHM5 deficiency alleviates aortic aneurysm by regulating smooth muscle calcium homeostasis.

Bo Yang, Ting Xu, Qianqian Yang, Liangzhu Mo, Jianyi Huo, Taiyang Mu, Yating Zhi, Yun Du, Haojie Wang, Lingchuan Guo and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

17 authors.

Bo Yang *Department of Cardiology, The Fourth Affiliated Hospital of Soochow University, Cyrus Tang Medical Institute, Medical College of Soochow University, Suzhou 215028, China.
Ting Xu *Institute for Fetology, Department of Pathology, First Affiliated Hospital of Soochow University, Suzhou 215006, China.
Qianqian Yang *Institute for Fetology, Department of Pathology, First Affiliated Hospital of Soochow University, Suzhou 215006, China.ORCID 0009-0004-2565-3427
Liangzhu MoDepartment of Cardiology, The Fourth Affiliated Hospital of Soochow University, Cyrus Tang Medical Institute, Medical College of Soochow University, Suzhou 215028, China.
Jianyi HuoDepartment of Cardiology, The Fourth Affiliated Hospital of Soochow University, Cyrus Tang Medical Institute, Medical College of Soochow University, Suzhou 215028, China.
Taiyang MuDepartment of Cardiology, The Fourth Affiliated Hospital of Soochow University, Cyrus Tang Medical Institute, Medical College of Soochow University, Suzhou 215028, China.
Yating ZhiDepartment of Cardiology, The Fourth Affiliated Hospital of Soochow University, Cyrus Tang Medical Institute, Medical College of Soochow University, Suzhou 215028, China.
Yun DuDepartment of Cardiology, The Fourth Affiliated Hospital of Soochow University, Cyrus Tang Medical Institute, Medical College of Soochow University, Suzhou 215028, China.ORCID 0009-0004-8736-5324
Haojie WangDepartment of Cardiology, The Fourth Affiliated Hospital of Soochow University, Cyrus Tang Medical Institute, Medical College of Soochow University, Suzhou 215028, China.
Lingchuan GuoInstitute for Fetology, Department of Pathology, First Affiliated Hospital of Soochow University, Suzhou 215006, China.
Zhen ZhuDepartment of Cardiology, The Fourth Affiliated Hospital of Soochow University, Cyrus Tang Medical Institute, Medical College of Soochow University, Suzhou 215028, China.ORCID 0009-0000-3478-5932
Yulong FengDepartment of Cardiology, The Fourth Affiliated Hospital of Soochow University, Cyrus Tang Medical Institute, Medical College of Soochow University, Suzhou 215028, China.
Yu RuiDepartment of Cardiology, The Fourth Affiliated Hospital of Soochow University, Cyrus Tang Medical Institute, Medical College of Soochow University, Suzhou 215028, China.
Li ZhuDepartment of Laboratory Medicine, Suzhou Ninth Hospital Affiliated to Soochow University, Cyrus Tang Medical Institute, Medical College of Soochow University, Suzhou 215200, China.
William A CoetzeeDepartments of Pathology, Neuroscience and Physiology, Biochemistry and Molecular Pharmacology, Medicine, and New York University School of Medicine, New York, NY 10016.
Qinqin GaoInstitute for Fetology, Department of Pathology, First Affiliated Hospital of Soochow University, Suzhou 215006, China.
Hua-Qian YangDepartment of Cardiology, The Fourth Affiliated Hospital of Soochow University, Cyrus Tang Medical Institute, Medical College of Soochow University, Suzhou 215028, China.ORCID 0000-0002-9402-6222

Funding

High Level Personnel Project of Jiangsu Province JSSCBS20210696High Level Personnel Project of Jiangsu Province JSSCRC2022472High Level Personnel Project of Jiangsu Province JSSCTD202353Jiangsu Provincial Natural Science Foundation BK20221243Jiangsu Provincial Natural Science Foundation BK20221358MOST | National Natural Science Foundation of China (NSFC) 82270268MOST | National Natural Science Foundation of China (NSFC) 82271724
6 · The paper itself

Abstract

Ion channels are the second most common clinical drug target besides G protein-coupled receptors. Aneurysmal diseases pose a significant threat to human life. Novel drug targets for its treatment remain to be explored. We investigated the role of an ion channel, calcium homeostasis modulators 5 (CALHM5), on the development of aortic aneurysms. We characterized CALHM5 as a plasma membrane ion channel abundant in smooth muscle cells of both humans and mice, playing a pivotal role in regulating calcium homeostasis. Notably, CALHM5 deficiency suppressed the transcription of the L-type calcium channel (LTCC) pore-forming subunit by downregulating cAMP-response element binding proteins. This in turn diminished blood vessel contractility and decreased blood flow. Intriguingly, CALHM5 expression is downregulated in smooth muscle tissues of aortic aneurysm patients. Furthermore, CALHM5 deficiency was observed to ameliorate the development of abdominal aortic aneurysms in mice, partly by stimulating smooth muscle cell proliferation. CALHM5 emerges as an ion channel prominently expressed in arterial smooth muscles, serving as a physiological regulator of smooth muscle contraction and presenting itself as a promising therapeutic target for aortic aneurysms.

Indexed as

Aortic AneurysmCalciumCalcium ChannelsMuscle, Smooth, VascularAnimalsCalcium Channels, L-TypeCell ProliferationHomeostasisHumansMaleMiceMice, KnockoutMyocytes, Smooth MuscleCalciumCalcium ChannelsCalcium Channels, L-Typeaortic aneurysmcalcium homeostasision channelplasma membranesmooth muscle

Identifiers

PMID41894331
PMCPMC13038059

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.