Tissue injury, both sterile and non-sterile, leads to the activation of immune cells, including macrophages, neutrophils, and other innate and adaptive immune cells. Persistent activation of immune cells augments the inflammatory response and promotes profibrotic cascade activation by increasing the production of various growth factors, particularly TGF-ß. Dysregulated tissue repair leads to fibrosis, a leading cause of mortality globally. Immune cell activation in different organ fibrosis, from the heart (heart failure), liver (cirrhosis), kidneys (chronic kidney disease) to lungs (pulmonary fibrosis), share many similar molecular mechanisms. Recent advances in single-cell sequencing highlighted the pivotal role of immune cells in fibrosis propagation. Effective treatment for various fibrotic diseases, from cirrhosis to pulmonary fibrosis, is still lacking. Immune cell function is closely linked to its metabolism. Alternation in metabolism can promote immune cell polarization to either proinflammatory or profibrotic status. There are growing interests in targeting metabolic pathways to modulate immune cell function and ameliorate fibrosis progression.
The goal of this Research Topic is to enrich our understanding of metabolic changes in both innate and adaptive immune cells during fibrotic diseases, and how these changes modulate immune cell function. The collection also aims to explore potential therapeutic targets to attenuate fibrosis and examine novel compounds that modulate immunometabolism in fibrotic diseases.
This Research Topic calls for articles focusing on the following:
1) identifying metabolic derangement in immune cells among different fibrotic diseases in various organs, and how the derangement changes immune cell function
2) therapeutically targeting metabolic pathways to attenuate fibrosis development in preclinical models
3) clinical trials to evaluate medications with known metabolic pathway targets in fibrotic diseases
We invite you to submit original research articles or relevant topic reviews on immunometabolism in fibrotic diseases.
Tissue injury, both sterile and non-sterile, leads to the activation of immune cells, including macrophages, neutrophils, and other innate and adaptive immune cells. Persistent activation of immune cells augments the inflammatory response and promotes profibrotic cascade activation by increasing the production of various growth factors, particularly TGF-ß. Dysregulated tissue repair leads to fibrosis, a leading cause of mortality globally. Immune cell activation in different organ fibrosis, from the heart (heart failure), liver (cirrhosis), kidneys (chronic kidney disease) to lungs (pulmonary fibrosis), share many similar molecular mechanisms. Recent advances in single-cell sequencing highlighted the pivotal role of immune cells in fibrosis propagation. Effective treatment for various fibrotic diseases, from cirrhosis to pulmonary fibrosis, is still lacking. Immune cell function is closely linked to its metabolism. Alternation in metabolism can promote immune cell polarization to either proinflammatory or profibrotic status. There are growing interests in targeting metabolic pathways to modulate immune cell function and ameliorate fibrosis progression.
The goal of this Research Topic is to enrich our understanding of metabolic changes in both innate and adaptive immune cells during fibrotic diseases, and how these changes modulate immune cell function. The collection also aims to explore potential therapeutic targets to attenuate fibrosis and examine novel compounds that modulate immunometabolism in fibrotic diseases.
This Research Topic calls for articles focusing on the following:
1) identifying metabolic derangement in immune cells among different fibrotic diseases in various organs, and how the derangement changes immune cell function
2) therapeutically targeting metabolic pathways to attenuate fibrosis development in preclinical models
3) clinical trials to evaluate medications with known metabolic pathway targets in fibrotic diseases
We invite you to submit original research articles or relevant topic reviews on immunometabolism in fibrotic diseases.
