Evidence map›Paper›PMID 42811065›Full record

ArticleNature communications2026

Pulsed electromagnetic fields activate a peripheral interoceptive pathway to suppress sympathetic Npy for osteogenesis.

Tiantian Wang, Zejun Liang, Wenjuan Zeng, Jiehao Chen, Changyi Wang, Xue Gong, Sihan Chen, Yaojia Zhou, Hongbin Wu, Linqiao Tang and 3 more

Abstract read
In one paragraph

Article in Nature communications, 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

13 authors.

Tiantian WangDepartment of Neurology, Institute of Neurology, West China Hospital of Sichuan University, Chengdu, Sichuan, China. 2352837518@qq.com.ORCID 0000-0002-7623-7245
Zejun LiangDepartment of Radiology, West China Hospital, Sichuan University, Chengdu, Sichuan, People's Republic of China.
Wenjuan ZengTransplantation Center & Institute of Organ Transplantation, NHC Key Lab of Transplant Engineering and Immunology, Institutes for Systems Genetics, Frontiers Science Center for Disease-Related Molecular Network, West China Hospital, Sichuan University, Chengdu, China.
Jiehao ChenAnimal Laboratory Center, West China Hospital, Sichuan University, Chengdu, Sichuan, People's Republic of China.
Changyi WangDepartment of Rehabilitation Medicine Center, West China Hospital, Sichuan University, Chengdu, Sichuan, People's Republic of China.ORCID 0000-0003-3153-9458
Xue GongDepartment of Psychiatry, Gansu Provincial Hospital, Lanzhou, People's Republic of China.
Sihan ChenDepartment of Neurology, Institute of Neurology, West China Hospital of Sichuan University, Chengdu, Sichuan, China.ORCID 0009-0001-6771-6156
Yaojia ZhouAnimal Laboratory Center, West China Hospital, Sichuan University, Chengdu, Sichuan, People's Republic of China.
Hongbin WuAnimal Laboratory Center, West China Hospital, Sichuan University, Chengdu, Sichuan, People's Republic of China.
Linqiao TangResearch Core Facility of West China Hospital, Sichuan University, Chengdu, Sichuan, P. R. China.
Yaru MaDepartment of Neurology, Institute of Neurology, West China Hospital of Sichuan University, Chengdu, Sichuan, China.
Dong ZhouDepartment of Neurology, Institute of Neurology, West China Hospital of Sichuan University, Chengdu, Sichuan, China.ORCID 0000-0001-7101-4125
Zhen HongDepartment of Neurology, Institute of Neurology, West China Hospital of Sichuan University, Chengdu, Sichuan, China. hongzhengoog@aliyun.com.ORCID 0000-0002-0014-6873

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82102656National Natural Science Foundation of China (National Science Foundation of China) 82402974National Natural Science Foundation of China (National Science Foundation of China) 82471388National Natural Science Foundation of China (National Science Foundation of China) U21A20393
6 · The paper itself

Abstract

Chronic stress-induced osteoporosis is a prevalent yet therapeutically challenging condition, with sympathetic overactivation as a key contributor. The dominant pathological mediator and strategies for its precise, non-invasive modulation remain unclear. Here, we identify sympathetic neuropeptide Y as a critical driver of this pathology. Using an unpredictable chronic mild stress model in male mice, we show that neuropeptide Y directly induces cellular senescence in bone marrow adipocytes, thereby impairing osteogenesis. Pulsed electromagnetic field treatment rescued bone loss in wild-type mice, but not in mice with sympathetic neuron-specific deletion of neuropeptide Y (Th

Indexed as

Electromagnetic FieldsNeuropeptide YOsteogenesisOsteoporosisSympathetic Nervous SystemAdipocytesAnimalsCellular SenescenceMaleMiceMice, Inbred C57BLReceptors, Neuropeptide YSemaphorin-3ASignal TransductionNeuropeptide Yneuropeptide Y-Y1 receptorReceptors, Neuropeptide YSemaphorin-3A

Identifiers

PMID42811065
PMCPMC13624269

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.