Fibrotic diseases that afflict the liver, lungs, kidneys, intestines, heart, and many other organs are a major cause of global morbidity and mortality. Tissue injury caused by infectious agents, toxic chemicals and inflammatory conditions elicit a repair process. Tissue repair is accompanied by the activation of mesenchymal cells that become myofibroblasts and produce extracellular matrix components. However, persistence of the inflammatory stimuli and impairment of the control mechanisms that regulate tissue repair can cause excess fibrosis and progressive loss of organ functions.
Tissue resident and monocyte-derived macrophages are key players in fibrogenesis and its resolution. Neutrophils, lymphocytes, NK cells and other immune cells that are recruited to the inflammatory site also impact tissue fibrosis. The immune cells engage in a bidirectional dialogue with fibroblasts to facilitate tissue repair. These cellular interactions are deregulated during progression toward fibrosis.
Impressive advances have been made in understanding the signaling pathways that promote fibroblast differentiation and matrix production, cytokines and growth factors that modulate immune cell activation and function, and chemokines that recruit immune cells. Development of new mouse models and in vitro assay systems have also played an instrumental role in this progress. The growing knowledge on the immunoregulatory networks in fibrosis has dispelled the notion that it is an irreversible condition and has opened promising new avenues for therapeutic modulation.
This special issue will focus on new advances in cellular and molecular aspects of immune cells related to fibrotic diseases but not limited to their crosstalk with mesenchymal cells in the development, resolution, and progression of tissue fibrosis. New studies on these topics in all target organs of tissue fibrosis are encouraged.
We welcome contributions in the form of Original Research, Brief Research Report, (Mini) Review, Perspective as well as Hypothesis pertaining but not limited to the following topics in the fibrotic diseases:
• Immune cell functions in fibrogenesis and its resolution.
• Crosstalk between fibroblasts and immune cells in tissue fibrosis.
• Experimental models of fibrogenesis and its resolution.
• Biomarkers and therapeutic strategies for fibrotic diseases
Fibrotic diseases that afflict the liver, lungs, kidneys, intestines, heart, and many other organs are a major cause of global morbidity and mortality. Tissue injury caused by infectious agents, toxic chemicals and inflammatory conditions elicit a repair process. Tissue repair is accompanied by the activation of mesenchymal cells that become myofibroblasts and produce extracellular matrix components. However, persistence of the inflammatory stimuli and impairment of the control mechanisms that regulate tissue repair can cause excess fibrosis and progressive loss of organ functions.
Tissue resident and monocyte-derived macrophages are key players in fibrogenesis and its resolution. Neutrophils, lymphocytes, NK cells and other immune cells that are recruited to the inflammatory site also impact tissue fibrosis. The immune cells engage in a bidirectional dialogue with fibroblasts to facilitate tissue repair. These cellular interactions are deregulated during progression toward fibrosis.
Impressive advances have been made in understanding the signaling pathways that promote fibroblast differentiation and matrix production, cytokines and growth factors that modulate immune cell activation and function, and chemokines that recruit immune cells. Development of new mouse models and in vitro assay systems have also played an instrumental role in this progress. The growing knowledge on the immunoregulatory networks in fibrosis has dispelled the notion that it is an irreversible condition and has opened promising new avenues for therapeutic modulation.
This special issue will focus on new advances in cellular and molecular aspects of immune cells related to fibrotic diseases but not limited to their crosstalk with mesenchymal cells in the development, resolution, and progression of tissue fibrosis. New studies on these topics in all target organs of tissue fibrosis are encouraged.
We welcome contributions in the form of Original Research, Brief Research Report, (Mini) Review, Perspective as well as Hypothesis pertaining but not limited to the following topics in the fibrotic diseases:
• Immune cell functions in fibrogenesis and its resolution.
• Crosstalk between fibroblasts and immune cells in tissue fibrosis.
• Experimental models of fibrogenesis and its resolution.
• Biomarkers and therapeutic strategies for fibrotic diseases
