ArticleJACC. Basic to translational science2025
FNDC4 Prevents Aging-Related Cardiac Dysfunction: By Restoring AMPKα/PPARα-Dependent Mitochondrial Function.
Article in JACC. Basic to translational science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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.
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Who cites it
1 citing paper in PubMed.
- Potential Molecular Mechanism of FNDC4 Protection Against Aging in the Heart.JACC. Basic to translational science · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria play critical roles in maintaining oxidative metabolism and cardiac homeostasis; however, their function is compromised in aging hearts. Fibronectin type III domain-containing 4 (FNDC4) is involved in regulating mitochondrial biogenesis, energy expenditure, and metabolic balance. The present study found that aging mice exhibited a sizable decline in cardiac and plasma FNDC4 levels, and that lower FNDC4 expression also correlated with a poor cardiac function. Cardiac-specific FNDC4 overexpression alleviated, while cardiac-specific FNDC4 knockdown facilitated aging-related cardiac remodeling and dysfunction. The unbiased transcriptome analysis and untargeted metabolomics revealed that FNDC4 activated AMP-activated protein kinase α/peroxisome proliferator-activated receptor α signaling pathway to improve mitochondrial dysfunction and lipotoxicity in aging hearts.
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Registered trials
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