Evidence map›Paper›PMID 37937441›Full record

ArticleCirculation2023

Polycystic Ovary Syndrome Fuels Cardiovascular Inflammation and Aggravates Ischemic Cardiac Injury.

Ling Gao, Yichao Zhao, Haiyan Wu, Xianhua Lin, Fei Guo, Jie Li, Yuhang Long, Bokang Zhou, Junsen She, Chen Zhang and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Circulation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 6 pooled it
20.8field-weighted citation impact, top 1% 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

56 citing papers in PubMed, 6 syntheses or guidelines pooled it, 76 citations in OpenAlex.

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  4. Non-coding rnas in Turner syndrome: a systematic review.Revista paulista de pediatria : orgao oficial da Sociedade de Pediatria de Sao Paulo · 2024
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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

14 authors at 6 institutions in 3 countries.

Ling Gao *Obstetrics and Gynecology Hospital, Institute of Reproduction and Development, Fudan University, Shanghai, China (L.G., X.L., F.G., J.L., Y.L., B.Z., C.Z., L.J., Y.W., H.H.).
Yichao Zhao *Department of Cardiology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China (Y.Z.).
Haiyan Wu *Key Laboratory of Reproductive Genetics (Ministry of Education), Women's Hospital, Zhejiang University School of Medicine, Hangzhou, China (L.G., H.W., J. She, H.H.).
Xianhua LinObstetrics and Gynecology Hospital, Institute of Reproduction and Development, Fudan University, Shanghai, China (L.G., X.L., F.G., J.L., Y.L., B.Z., C.Z., L.J., Y.W., H.H.).
Fei GuoObstetrics and Gynecology Hospital, Institute of Reproduction and Development, Fudan University, Shanghai, China (L.G., X.L., F.G., J.L., Y.L., B.Z., C.Z., L.J., Y.W., H.H.).
Jie LiObstetrics and Gynecology Hospital, Institute of Reproduction and Development, Fudan University, Shanghai, China (L.G., X.L., F.G., J.L., Y.L., B.Z., C.Z., L.J., Y.W., H.H.).
Yuhang LongObstetrics and Gynecology Hospital, Institute of Reproduction and Development, Fudan University, Shanghai, China (L.G., X.L., F.G., J.L., Y.L., B.Z., C.Z., L.J., Y.W., H.H.).ORCID 0000-0002-5751-805X
Bokang ZhouObstetrics and Gynecology Hospital, Institute of Reproduction and Development, Fudan University, Shanghai, China (L.G., X.L., F.G., J.L., Y.L., B.Z., C.Z., L.J., Y.W., H.H.).
Junsen SheKey Laboratory of Reproductive Genetics (Ministry of Education), Women's Hospital, Zhejiang University School of Medicine, Hangzhou, China (L.G., H.W., J. She, H.H.).
Chen ZhangObstetrics and Gynecology Hospital, Institute of Reproduction and Development, Fudan University, Shanghai, China (L.G., X.L., F.G., J.L., Y.L., B.Z., C.Z., L.J., Y.W., H.H.).ORCID 0000-0003-3556-6752
Jianzhong ShengInternational Institutes of Medicine, the Fourth Affiliated Hospital, Zhejiang University School of Medicine, Yiwu, China (J. Sheng, H.H.).
Li JinObstetrics and Gynecology Hospital, Institute of Reproduction and Development, Fudan University, Shanghai, China (L.G., X.L., F.G., J.L., Y.L., B.Z., C.Z., L.J., Y.W., H.H.).
Yanting WuObstetrics and Gynecology Hospital, Institute of Reproduction and Development, Fudan University, Shanghai, China (L.G., X.L., F.G., J.L., Y.L., B.Z., C.Z., L.J., Y.W., H.H.).
Hefeng HuangObstetrics and Gynecology Hospital, Institute of Reproduction and Development, Fudan University, Shanghai, China (L.G., X.L., F.G., J.L., Y.L., B.Z., C.Z., L.J., Y.W., H.H.).
Obstetrics and Gynecology Hospital of Fudan University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNMinistry of Education · THMinistry of Education · KRRenji Hospital · CNSheng Jing Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundReducing cardiovascular disease burden among women remains challenging. Epidemiologic studies have indicated that polycystic ovary syndrome (PCOS), the most common endocrine disease in women of reproductive age, is associated with an increased prevalence and extent of coronary artery disease. However, the mechanism through which PCOS affects cardiac health in women remains unclear.

methodsPrenatal anti-Müllerian hormone treatment or peripubertal letrozole infusion was used to establish mouse models of PCOS. RNA sequencing was performed to determine global transcriptomic changes in the hearts of PCOS mice. Flow cytometry and immunofluorescence staining were performed to detect myocardial macrophage accumulation in multiple PCOS models. Parabiosis models, cell-tracking experiments, and in vivo gene silencing approaches were used to explore the mechanisms underlying increased macrophage infiltration in PCOS mouse hearts. Permanent coronary ligation was performed to establish myocardial infarction (MI). Histologic analysis and small-animal imaging modalities (eg, magnetic resonance imaging and echocardiography) were performed to evaluate the effects of PCOS on injury after MI. Women with PCOS and control participants (n=200) were recruited to confirm findings observed in animal models.

resultsTranscriptomic profiling and immunostaining revealed that hearts from PCOS mice were characterized by increased macrophage accumulation. Parabiosis studies revealed that monocyte-derived macrophages were significantly increased in the hearts of PCOS mice because of enhanced circulating Ly6C

conclusionsOur data documented previously unrecognized mechanisms through which PCOS could affect cardiovascular health in women. PCOS may promote myocardial macrophage accumulation and post-MI cardiac remodeling because of augmented splenic myelopoiesis.

Indexed as

Heart InjuriesMyocardial InfarctionPolycystic Ovary SyndromeAnimalsFemaleHumansInflammationMiceNorepinephrinePregnancyVentricular RemodelingNorepinephrineatherosclerotic plaqueimmunitymacrophagesmonocytesmyocardial infarctionpolycystic ovary syndrome

Identifiers

PMID37937441
PMCPMC10713005
OpenAlexW4388493738

What OpenQuestion holds

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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.