ArticleNature communications2025
Adipose tissue-derived PRXL2A suppresses hepatic lipogenesis in a study with male mice.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed.
- Mechanisms and therapeutic potential of AMPK signaling pathway in the regulation of lipid metabolism.Molecular biology reports · 2026Review
- KNL1 Regulates Ferroptosis Resistance and Migration in Lung Adenocarcinoma Cells via AMPK-mTOR Signaling.Oncology research · 2026Article
- Resveratrol Impairs Insulin Signaling in Hepatic Cells via Activation of PKC and PTP1B Pathways.International journal of molecular sciences · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
Hepatic de novo lipogenesis (DNL) is crucial for maintaining lipid homeostasis, and its dysregulation is implicated in various metabolic diseases. While it is well established that hepatic DNL is tightly regulated by hormones such as insulin and glucagon secreted from the pancreatic islets during feeding and fasting, further investigations are required to identify more hormones affecting hepatic DNL during the feeding-fasting transition. Here, we identify PRXL2A (peroxiredoxin like 2 A), an adipokine secreted during fasting, as an inhibitor of hepatic DNL. Mechanistically, PRXL2A binds to its receptor PTAFR (platelet activating factor receptor), promoting calcium mobilization and activating AMPK (AMP-activated protein kinase), thereby suppressing SREBP1 (sterol regulatory element-binding protein 1)-controlled hepatic DNL. Disruption of this axis by knockout of either Prxl2a or Ptafr increases hepatic DNL and lipid accumulation. Exogenous PRXL2A reduces hepatic DNL, suggesting a potential therapeutic strategy for diseases associated with hepatic lipid accumulation. Therefore, the PRXL2A-PTAFR signaling axis links adipose tissues and the liver to regulate hepatic lipid metabolism.
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