ArticleInternational journal of obesity (2005)2024
Asprosin contributes to pathogenesis of obesity by adipocyte mitophagy induction to inhibit white adipose browning in mice.
Article in International journal of obesity (2005), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Circular RNAs in metabolic health: bridging the gap between molecular biology and therapy.Cell death & disease · 2026Review
- Article
- Asprosin Protects H9C2 Cells From Ferroptosis Following Hypoxia/Reoxygenation by Promoting Mitophagy.Cardiovascular therapeutics · 2026Article
- WDR4-mediate tRNA m7G modification to promote mitophagy and browning of white adipose tissue for ameliorating obesity in male mice.Adipocyte · 2025Article
- Associations between asprosin, insulin resistance, and oxidative stress in adults with obesity.Scientific reports · 2025Article
- The Adipokine Hypothesis of Heart Failure With a Preserved Ejection Fraction: A Novel Framework to Explain Pathogenesis and Guide Treatment.Journal of the American College of Cardiology · 2025Review
- Asprosin Aggravates Tubular Epithelial Cell Injury and Phenotypic Transformation via Mitochondrial Dynamics Disorder Mediated by Excessive Drp1 SUMOylation in Diabetic Nephropathy Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Pathophysiological insights into asprosin: an emerging adipokine in reproductive health.Reviews in endocrine & metabolic disorders · 2025Review
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Authors and funding
11 authors.
Funding
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Abstract
backgroundAsprosin (ASP) is a newly discovered adipokine secreted by white adipose tissue (WAT), which can regulate the homeostasis of glucose and lipid metabolism. However, it is not clear whether it can regulate the browning of WAT and mitophagy during the browning process. Accordingly, this study aims to investigate the effects and possible mechanisms of ASP on the browning of WAT and mitophagy in vivo and in vitro.
methodsIn in vivo experiments, some mouse models were used including adipose tissue ASP-specific deficiency (ASP
resultsOur in vivo data show that adipose tissue-specific deletion of ASP contributes to weight loss in mice; supplementation of ASP inhibits the expressions of browning-related proteins including UCP1, PRDM16 and PGC1ɑ during the cold exposure-induced browning, and promotes the expressions of mitophagy-related proteins including PINK1 and Parkin under the conditions of whether normal diet (ND) or HFD. Similarly, our in vitro data also show that the deletion of ASP in 3T3-L1 cells significantly increases the expressions of the browning-related proteins and decreases the expressions of the mitophagy-related proteins.
conclusionsThese data demonstrate that ASP deletion can facilitate the browning and inhibit mitophagy in WAT. The findings will lay an experimental foundation for the development of new drugs targeting ASP and the clinical treatment of metabolic diseases related to obesity.
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