Evidence mapPaperPMID 41009040Full record

ReviewAntioxidants (Basel, Switzerland)2025

Impact of Maternal High-Fat Diet on Offspring Cardiovascular-Kidney-Metabolic Health: Spotlight on Oxidative Stress.

Chien-Ning Hsu, Chih-Kuang Chen, Chih-Yao Hou, Yu-Wei Chen, Guo-Ping Chang-Chien, Shu-Fen Lin, You-Lin Tain

Abstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. 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

7 authors.

Chien-Ning HsuDepartment of Pharmacy, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 833, Taiwan.ORCID 0000-0001-7470-528X
Chih-Kuang ChenPolymeric Biomaterials Laboratory, Department of Materials and Optoelectronic Science, National Sun Yat-sen University, Kaohsiung 804, Taiwan.ORCID 0000-0002-7896-2424
Chih-Yao HouDepartment of Seafood Science, National Kaohsiung University of Science and Technology, Kaohsiung 811, Taiwan.ORCID 0000-0002-8007-6077
Yu-Wei ChenDepartment of Food Science and Biotechnology, National Chung Hsing University, Taichung 402, Taiwan.
Guo-Ping Chang-ChienCenter for Environmental Toxin and Emerging-Contaminant Research, Cheng Shiu University, Kaohsiung 833, Taiwan.ORCID 0000-0003-3560-7470
Shu-Fen LinCenter for Environmental Toxin and Emerging-Contaminant Research, Cheng Shiu University, Kaohsiung 833, Taiwan.
You-Lin TainDepartment of Pediatrics, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 833, Taiwan.ORCID 0000-0002-7059-6407

Funding

National Science and Technology Council, Taiwan 114-2314-B-182A-036-MY3 and 114-2314-B-182A-048National Sun Yat-Sen University, Taiwan CGMH-NSYSU-114-P01
6 · The paper itself

Abstract

Cardiovascular-kidney-metabolic syndrome (CKMS) encompasses interconnected cardiovascular, renal, and metabolic disorders, including obesity, hypertension, and type 2 diabetes. Oxidative stress is increasingly recognized as a central driver of this multi-organ dysfunction. Among maternal influences, exposure to a high-fat diet (HFD) during pregnancy and lactation consistently predisposes offspring to CKMS-related phenotypes in animal models. While oxidative stress is implicated as a key mediator, its precise role in developmental programming remains unclear, and comparing the differences in its role between overt CKMS and CKM programming is critical. Critical gaps include whether oxidative stress acts uniformly or in an organ- and time-specific manner, which signals initiate long-term redox alterations, and whether these effects are reversible. Furthermore, its interactions with other programming pathways-such as renin-angiotensin system activation, epigenetic dysregulation, gut microbiota imbalance, and altered nutrient sensing-remain insufficiently explored. This review uniquely highlights maternal HFD-induced oxidative stress as a mechanistic axis of CKMS programming and delineates unresolved questions that limit translation. By integrating evidence across organ systems and proposing priorities for multi-organ profiling, refined models, and longitudinal human studies, we outline a forward-looking agenda for the field. Ultimately, clarifying how maternal HFD and oxidative stress shape offspring CKMS risk is essential to inform targeted antioxidant strategies to reduce the intergenerational transmission of CKMS risk.

Indexed as

antioxidantscardiovascular diseasechronic kidney diseasedevelopmental origins of health and disease (DOHaD)diabeteshigh-fat diethypertensionmetabolic syndromeobesityoxidative stress

Identifiers

PMID41009040
PMCPMC12466590

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.