Chronic inflammatory reactions could be induced by a variety of stimuli, including tissue injury, infections, allergies and autoimmunity. Fibrosis, characterized by the excessive production and deposition of extracellular matrix (ECM), is the end result of chronic inflammatory reactions. Fibrosis can affect many organs such as the liver, lungs and kidneys and might eventually lead to permanent scarring, organ malfunction and death. Organ malfunction is frequently caused by fibrotic tissue remodeling, which is also often linked to high morbidity and mortality. In effect, up to 45% of all fatalities in the industrialized world are caused by fibrosis.
The goal of this Research Topic is to identify biological targets that can inhibit fibrotic and inflammatory pathways, which is a common challenge in fibrosis therapy. The collection will include manuscripts focusing on the modulation of key signaling pathways, redox imbalance and other processes implicated in the pathogenesis of chronic inflammation and fibrogenesis. Submissions describing cutting-edge research on the pathogenesis and biological interactions between new drug candidates and the claimed targets are highly recommended.
We welcome Original Research, Review, Mini Review and Perspective articles on themes including, but not limited to:
• The interplay between inflammatory reactions and fibrogenesis
• The altered pathways implicated in fibrogenesis
• The promising targets for treatment fibrotic diseases
• New assays and markers for the early detection of fibrotic changes
• Lead optimization to maximize the potency and selectivity against the inflammation and fibrosis pathways
• In vitro and in vivo biological evaluation of the target markers
Chronic inflammatory reactions could be induced by a variety of stimuli, including tissue injury, infections, allergies and autoimmunity. Fibrosis, characterized by the excessive production and deposition of extracellular matrix (ECM), is the end result of chronic inflammatory reactions. Fibrosis can affect many organs such as the liver, lungs and kidneys and might eventually lead to permanent scarring, organ malfunction and death. Organ malfunction is frequently caused by fibrotic tissue remodeling, which is also often linked to high morbidity and mortality. In effect, up to 45% of all fatalities in the industrialized world are caused by fibrosis.
The goal of this Research Topic is to identify biological targets that can inhibit fibrotic and inflammatory pathways, which is a common challenge in fibrosis therapy. The collection will include manuscripts focusing on the modulation of key signaling pathways, redox imbalance and other processes implicated in the pathogenesis of chronic inflammation and fibrogenesis. Submissions describing cutting-edge research on the pathogenesis and biological interactions between new drug candidates and the claimed targets are highly recommended.
We welcome Original Research, Review, Mini Review and Perspective articles on themes including, but not limited to:
• The interplay between inflammatory reactions and fibrogenesis
• The altered pathways implicated in fibrogenesis
• The promising targets for treatment fibrotic diseases
• New assays and markers for the early detection of fibrotic changes
• Lead optimization to maximize the potency and selectivity against the inflammation and fibrosis pathways
• In vitro and in vivo biological evaluation of the target markers
