Evidence map›Paper›PMID 42194089›Full record

ArticleBiomolecules2026

Up-Regulation of the TRPM8 Channel Attenuates TRPC1-Mediated Store-Operated Calcium Entry in Abdominal Aortic Aneurysm.

Yi-Qian Wang, Min Pan, Yi-Chen Lin, Si-Yi Zheng, Qin-Ye Chen, Long-Xin Gui, Mo-Jun Lin, Da-Cen Lin

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biomolecules, 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

8 authors.

Yi-Qian WangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou 350122, China.
Min PanDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou 350122, China.
Yi-Chen LinKey Laboratory of Fujian Province Universities on Ion Channel and Signal Transduction in Cardiovascular Diseases, Fujian Medical University, Fuzhou 350122, China.
Si-Yi ZhengKey Laboratory of Fujian Province Universities on Ion Channel and Signal Transduction in Cardiovascular Diseases, Fujian Medical University, Fuzhou 350122, China.
Qin-Ye ChenDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou 350122, China.
Long-Xin GuiDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou 350122, China.
Mo-Jun LinDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou 350122, China.
Da-Cen LinKey Laboratory of Fujian Province Universities on Ion Channel and Signal Transduction in Cardiovascular Diseases, Fujian Medical University, Fuzhou 350122, China.ORCID 0000-0001-9222-3719

Funding

Ion Channel and Signal Transduction in Cardiovascular Diseases, Fujian Medical University FMUISCD-202301National Natural Science Foundation of China 32571312National Natural Science Foundation of China 82203354the Innovation of Science and Technology, Fujian Province 2023Y9105the Innovation of Science and Technology, Fujian Province 2025Y9269
6 · The paper itself

Abstract

Abdominal aortic aneurysm (AAA) is a life-threatening vascular disease characterized by vascular smooth muscle cell (VSMC) dysfunction and disrupted calcium homeostasis. While transient receptor potential canonical 6 (TRPC6) and transient receptor potential canonical 1 (TRPC1) are known to mediate receptor-operated calcium entry (ROCE) and store-operated calcium entry (SOCE), respectively, the specific contributions of SOCE and ROCE to AAA pathogenesis, and the regulatory interaction between transient receptor potential melastatin 8 (TRPM8) and TRPC1 remain unexplored. In this study, we analyzed human AAA tissues, a papain-induced mouse model, and angiotensin II (Ang II)-treated human aortic smooth muscle cells using histology, wire myography, calcium imaging, and patch-clamp electrophysiology. We observed significant upregulation of TRPM8, TRPC1, and TRPC6 in both human and experimental AAA, with TRPC1 identified as a key mediator of SOCE under pathological conditions. Pharmacological activation of TRPM8 by menthol attenuated TRPC1-mediated SOCE and associated vasoconstriction, effects that were partially reversed by the TRPM8 antagonist A-2. In Ang II-treated cells, TRPM8 activation reduced SOCE and store-operated calcium currents (I

Indexed as

Aortic Aneurysm, AbdominalCalciumTRPC Cation ChannelsTRPM Cation ChannelsUp-RegulationAngiotensin IIAnimalsHumansMaleMiceMuscle, Smooth, VascularMyocytes, Smooth MuscleAngiotensin IICalciumtransient receptor potential cation channel, subfamily C, member 1TRPC Cation ChannelsTRPM8 protein, humanTRPM Cation Channelsabdominal aortic aneurysmstore-operated calcium entryTRPC1TRPM8vascular smooth muscle cells

Identifiers

PMID42194089
PMCPMC13204588

What Socratic holds

Textmetadata
LicenceCC BY
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.