ArticleJournal of animal science and biotechnology2025
Proteomics and cytokine array jointly reveal the role of macrophage proinflammatory shift in liver fibrosis in dairy cows with ketosis.
Article in Journal of animal science and biotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Natural Product Treatment for Metabolic Dysfunction-Associated Steatotic Liver Disease: Targeted Mitochondrial Quality Control.Drug design, development and therapy · 2026Review
- Microbiota-derived indole-3-acetic acid alleviates rumen epithelial barrier dysfunction during the peripartum period through AhR signaling.NPJ biofilms and microbiomes · 2025Article
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9 authors.
Funding
Abstract
backgroundChanges in macrophage function are crucial contributors to hepatic inflammation and fibrosis. However, the role of macrophages in the development of liver fibrosis in dairy cows with ketosis remains unclear. This study integrated proteomics and cytokine array approach to identify the multifactorial and multicellular interaction effects driving liver fibrosis in dairy cows with ketosis and analyze the mechanism by which the proinflammatory shift in macrophages contributes to liver fibrosis.
resultsHistopathological analysis revealed liver injury, including severe steatosis, infiltration of inflammatory cells, an increase in lipid deposition, and a decrease in glycogen expression in ketotic cows. Moreover, the number of mitochondria considerably increased in hepatocytes. The activation of the dynamin-related protein 1/mitochondrial fission factor (DRP1/MFF) pathway induced excessive mitochondrial fission, and the inhibition of the nuclear factor erythroid 2-related factor 2/heme oxygenase 1 (Nrf2/HO-1) pathway led to the accumulation of intracellular reactive oxygen species (ROS). Proteomic analysis revealed the activation of extracellular matrix (ECM)-related functions and the NF-κB pathway in the liver, whereas cytokine array analysis revealed that the cytokine network was dysregulated. The accumulation of ROS triggered NF-κB nuclear translocation, inducing a proinflammatory shift in macrophages and liver inflammation. M1 polarization of macrophages promotes the release of proinflammatory mediators, which stimulated hepatic stellate cells (HSCs) activation, leading to ECM deposition, ultimately contributing to liver fibrosis.
conclusionsTo summarize, our study revealed the multifactorial and multicellular interaction effects driving liver fibrosis. Our results preliminarily showed that increased mitochondrial fission and inhibition of the Nrf2/HO-1 pathway are key factors in activating macrophages, which can lead to liver fibrosis in dairy cows with ketosis.
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