Evidence map›Paper›PMID 38205641›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2024

FSH Is Responsible for Androgen Deprivation Therapy-Associated Atherosclerosis in Mice by Exaggerating Endothelial Inflammation and Monocyte Adhesion.

Qiang Wang, Jingli Han, Zhenhui Liang, Xueyu Geng, Yiqing Du, Jing Zhou, Weijuan Yao, Tao Xu

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
7.9field-weighted citation impact, top 2% of its field
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

15 citing papers in PubMed, 22 citations in OpenAlex.

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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 at 2 institutions in 2 countries.

Qiang Wang *Department of Urology, Peking University People's Hospital, Beijing, China (Q.W., J.H., Y.D., T.X.).ORCID 0000-0001-9504-4302
Jingli Han *Department of Urology, Peking University People's Hospital, Beijing, China (Q.W., J.H., Y.D., T.X.).ORCID 0009-0001-2683-7031
Zhenhui Liang *Department of Physiology and Pathophysiology, Hemorheology Center, School of Basic Medical Sciences, Peking University, Beijing, China (Z.L., X.G., J.Z., W.Y.).ORCID 0009-0001-2764-2375
Xueyu GengDepartment of Physiology and Pathophysiology, Hemorheology Center, School of Basic Medical Sciences, Peking University, Beijing, China (Z.L., X.G., J.Z., W.Y.).ORCID 0009-0009-1524-8539
Yiqing DuDepartment of Urology, Peking University People's Hospital, Beijing, China (Q.W., J.H., Y.D., T.X.).ORCID 0000-0002-5089-727X
Jing ZhouDepartment of Physiology and Pathophysiology, Hemorheology Center, School of Basic Medical Sciences, Peking University, Beijing, China (Z.L., X.G., J.Z., W.Y.).ORCID 0000-0002-2211-4901
Weijuan YaoDepartment of Physiology and Pathophysiology, Hemorheology Center, School of Basic Medical Sciences, Peking University, Beijing, China (Z.L., X.G., J.Z., W.Y.).ORCID 0000-0003-4698-612X
Tao XuDepartment of Urology, Peking University People's Hospital, Beijing, China (Q.W., J.H., Y.D., T.X.).ORCID 0000-0003-3899-1500
Ministry of Education of the People's Republic of China · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAndrogen deprivation therapy (ADT) is the mainstay treatment for advanced prostate cancer. But ADTs with orchiectomy and gonadotropin-releasing hormone (GnRH) agonist are associated with increased risk of cardiovascular diseases, which appears less significant with GnRH antagonist. The difference of follicle-stimulating hormone (FSH) in ADT modalities is hypothesized to be responsible for ADT-associated cardiovascular diseases.

methodsWe administered orchiectomy, GnRH agonist, or GnRH antagonist in male

resultsOrchiectomy and GnRH agonist, but not GnRH antagonist, induced long- or short-term FSH elevation and significantly accelerated atherogenesis. In orchiectomized and testosterone-supplemented mice, FSH exposure increased atherosclerosis. In GnRH agonist-treated mice, blocking of short FSH surge by anti-FSHβ antibody greatly alleviated endothelial inflammation and delayed atherogenesis. In GnRH antagonist-treated mice, FSH supplementation aggravated atherogenesis. Mechanistically, FSH, synergizing with TNF-α (tumor necrosis factor alpha), exacerbated endothelial inflammation by elevating VCAM-1 (vascular cell adhesion protein 1) expression through the cAMP/PKA (protein kinase A)/CREB (cAMP response element-binding protein)/c-Jun and PI3K (phosphatidylinositol 3 kinase)/AKT (protein kinase B)/GSK-3β (glycogen synthase kinase 3 beta)/GATA-6 (GATA-binding protein 6) pathways. In monocytes, FSH upregulated CD29 (cluster of differentiation 29) expression via the PI3K/AKT/GSK-3β/SP1 (specificity protein 1) pathway and promoted monocyte-endothelial adhesion both in vitro and in vivo. Importantly, FSHR knockdown by shRNA in endothelium of carotid arteries markedly reduced GnRH agonist-induced endothelial inflammation and atherosclerosis in mice.

conclusionsFSH is responsible for ADT-associated atherosclerosis by exaggerating endothelial inflammation and promoting monocyte-endothelial adhesion.

Indexed as

AtherosclerosisCardiovascular DiseasesProstatic NeoplasmsAndrogen AntagonistsAndrogensAnimalsEndotheliumFollicle Stimulating HormoneGlycogen Synthase Kinase 3 betaGonadotropin-Releasing HormoneInflammationMaleMiceMonocytesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAndrogen AntagonistsAndrogensFollicle Stimulating HormoneGlycogen Synthase Kinase 3 betaGonadotropin-Releasing HormonePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTestosteroneatherosclerosisendothelial cellsfollicle-stimulating hormonemonocytesprostatic neoplasms

Identifiers

PMID38205641
PMCPMC10880942
OpenAlexW4390743385

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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 OpenQuestion graph.