The results reveal in vivo, that 1) hepatocyte-specific Alk3 deficiency partly protects from AI, 2) the development of hypoferremia is partly dependent on ALK3, and 3) the ALK3/BMP/hepcidin axis may serve as a possible therapeutic target to attenuate AI.
Keyphrases
- advanced non small cell lung cancer
- artificial intelligence
- mesenchymal stem cells
- oxidative stress
- chronic kidney disease
- epidermal growth factor receptor
- replacement therapy
- iron deficiency
- genome wide
- single cell
- bone regeneration
- gene expression
- machine learning
- high fat diet induced
- skeletal muscle
- smoking cessation
- drug induced