Evidence map›Paper›PMID 41223853›Full record

ArticleCell reports. Medicine2025

Maternal diabetes programs sexually dimorphic early-onset cardiovascular dysfunction in metabolically healthy offspring.

Allan Zhao, Yuxia Wei, Eftychia Kontidou, Ali Mahdi, Paulo R Jannig, Sara Torstensson, Hong Jiang, Alice Larsson, Aida Collado, Rawan Humoud and 16 more

Abstract read
In one paragraph

Article in Cell reports. Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Review
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

26 authors.

Allan ZhaoDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden; Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.
Yuxia WeiInstitute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
Eftychia KontidouDivision of Cardiology, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
Ali MahdiDivision of Cardiology, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
Paulo R JannigDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden; Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.
Sara TorstenssonDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Hong JiangDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden; Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.
Alice LarssonDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Aida ColladoDivision of Cardiology, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
Rawan HumoudDivision of Cardiology, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
Jacob GrünlerDepartment of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
David ErsgårdDivision of Cardiology, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
Buket Öztürk EsenDepartment of Clinical Epidemiology and Center for Population Medicine, Aarhus University, Aarhus, Denmark.
Xiaowei ZhengDepartment of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
Haojiang LuDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Eva LindgrenDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Sanjiv RisalDepartment of Clinical Science, Intervention and Technology (CLINTEC), Karolinska Institutet, Stockholm, Sweden; Division of Obstetrics and Gynecology, Karolinska University Hospital, Stockholm, Sweden.
Jian ZhaoDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Elisabet Stener-VictorinDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Henrik Toft SørensenDepartment of Clinical Epidemiology and Center for Population Medicine, Aarhus University, Aarhus, Denmark.
Lars PedersenDepartment of Clinical Epidemiology and Center for Population Medicine, Aarhus University, Aarhus, Denmark.
John PernowDivision of Cardiology, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden; Department of Cardiology, Karolinska University Hospital, Stockholm, Sweden.
Zhichao ZhouDivision of Cardiology, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
Sofia CarlssonInstitute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
Sergiu-Bogdan CatrinaDepartment of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden; Center for Diabetes, Academic Specialist Center, Stockholm, Sweden.
Qiaolin DengDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden; Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden. Electronic address: qiaolin.deng@ki.se.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The incidence of cardiovascular disease (CVD) in young individuals is increasing. This alarming trend underscores the need to identify at-risk groups for preventive measures. Emerging evidence suggests that maternal diabetes increases the risk for metabolic diseases and early-onset CVDs in their offspring. However, the evidence is largely observational, limited by confounding factors, and lacks crucial mechanistic insight. Here, we combine experimental, epidemiological, and clinical approaches to disentangle the effects of maternal diabetes on offspring metabolism and endothelial function. In mice, we find that maternal hyperglycemia induces early-onset endothelial dysfunction specifically in male offspring, independent of metabolic disease. In humans, a case-control study and an epidemiological study confirm elevated risk of early-onset endothelial dysfunction and related CVDs in metabolically healthy sons of mothers with type 1 diabetes. Our findings identify an underrecognized risk group for early-onset CVDs and emphasize the importance of maternal conditions in shaping the cardiovascular health of future generations.

Indexed as

Cardiovascular DiseasesDiabetes, GestationalDiabetes Mellitus, Type 1Prenatal Exposure Delayed EffectsSex CharacteristicsAdultAnimalsCase-Control StudiesEndothelium, VascularFemaleHumansMaleMiceMice, Inbred C57BLPregnancyRisk Factorscardiovascular diseasedevelopmental programmingdiabetesDOHaDendothelial dysfunctioninheritancemetabolismoffspringsex dimorphism

Identifiers

PMID41223853
PMCPMC12711690

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.