ArticleCell & bioscience2023
Aging aggravates acetaminophen-induced acute liver injury and inflammation through inordinate C/EBPα-BMP9 crosstalk.
Article in Cell & bioscience, 2023. 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, 13 citations in OpenAlex.
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- Bone morphogenetic protein (BMP)-9, a systemic homeostasis factor with diverse functions in the liver and beyond.Bioscience reports · 2025Review
- Unveiling the Impact of BMP9 in Liver Diseases: Insights into Pathogenesis and Therapeutic Potential.Biomolecules · 2024Review
- Cellular Senescence in Acute Liver Injury: What Happens to the Young Liver?Aging and disease · 2024Review
- AIM2 regulates autophagy to mitigate oxidative stress in aged mice with acute liver injury.Cell death discovery · 2024Article
- MethylRAD Sequencing Technology Reveals DNA Methylation Characteristics ofAnimals : an open access journal from MDPI · 2023Article
- The Role of Inflammation in Cholestatic Liver Injury.Journal of inflammation research · 2023Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundPrevious studies have shown that bone morphogenetic protein 9 (BMP9) is almost exclusively produced in the liver and reaches tissues throughout the body as a secreted protein. However, the mechanism of BMP9 action and its role in aging-associated liver injury and inflammation are still unclear.
resultsAging significantly aggravates acetaminophen (APAP)-induced acute liver injury (ALI). Increased expression of CCAAT/enhancer binding protein α (C/EBPα) and BMP9 was identified in aged livers and in hepatocytes and macrophages (MФs) isolated from aged mice. Further analysis revealed that excess BMP9 was directly related to APAP-induced hepatocyte injury and death, as evidenced by activated drosophila mothers against decapentaplegic protein 1/5/9 (SMAD1/5/9) signaling, an increased dead cell/total cell ratio, decreased levels of ATG3 and ATG7, blocked autophagy, increased senescence-associated beta-galactosidase (SA-β-Gal) activity, and a higher rate of senescence-associated secretory phenotype (SASP) acquisition. In contrast, Bmp9 knockout (Bmp9
conclusionsIn summary, the present study highlights the crucial roles played by C/EBPα-BMP9 crosstalk and provides insights into the interrelationship between hepatocytes and MΦs during acute liver injury.
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