In adult mammals, tissue damage activates a wound healing response with acute inflammation followed by either complete repair (for low-grade damage or in highly regenerative tissues, such as the liver) or replacement fibrosis (for extensive damage or in poorly regenerative tissues, such as the myocardium). Persistent damage and repeated insults sustain continuous activation of repair pathways leading to chronic inflammation, progressive tissue fibrosis and sclerosis.
Despite the evolutionary advantage conferred by scarring as a rapid repair mechanism, chronic fibrosis leads to tissue adverse remodeling and impaired function.
Persistent low-level inflammation and fibrosis are observed in many pathological conditions (e.g. hypertension, obesity, diabetes, genetic diseases), and lead to further complications including atherosclerosis and ischemic events, organ failure, autoimmune diseases, cancer, aging, and reduced resilience to infectious diseases.
Pathological fibrosis plays a major role in a wide range of diseases, accounting for an increasingly large fraction of mortality cases worldwide. While recent advances have unveiled many environmental and genetic causes of fibrotic disorders, a better understanding of both ubiquitous and tissue-specific regulatory pathways and cellular dynamics could help to design new targeted therapies, and to identify the etiology of idiopathic diseases.
Within this Research Topic, we invite submission of articles (reviews, original research, or methodology articles) on the pathophysiological role of fibrosis and inflammation in different tissues. Areas to be covered include, but are not limited to:
- genetic and environmental causes of persistent low-level inflammation and fibrosis (e.g. autoimmunity, hypertension, obesity, diabetes, genetic diseases, latent infections);
- comorbidities including systemic sclerosis, neurological disorders, organ failure (heart, skeletal muscle, kidney, liver, lungs), cancer, and reduced resilience to infectious diseases;
- in vivo (animal models) and in vitro (organoids, tissue culture) modelling of fibrotic diseases for the discovery of novel therapeutic targets and potential tissue-specific treatments;
- vascular responses to inflammation and inflammation of vascular tissues;
- system biology approaches to identify molecular and cellular networks leading to chronic inflammation and fibrosis.
In adult mammals, tissue damage activates a wound healing response with acute inflammation followed by either complete repair (for low-grade damage or in highly regenerative tissues, such as the liver) or replacement fibrosis (for extensive damage or in poorly regenerative tissues, such as the myocardium). Persistent damage and repeated insults sustain continuous activation of repair pathways leading to chronic inflammation, progressive tissue fibrosis and sclerosis.
Despite the evolutionary advantage conferred by scarring as a rapid repair mechanism, chronic fibrosis leads to tissue adverse remodeling and impaired function.
Persistent low-level inflammation and fibrosis are observed in many pathological conditions (e.g. hypertension, obesity, diabetes, genetic diseases), and lead to further complications including atherosclerosis and ischemic events, organ failure, autoimmune diseases, cancer, aging, and reduced resilience to infectious diseases.
Pathological fibrosis plays a major role in a wide range of diseases, accounting for an increasingly large fraction of mortality cases worldwide. While recent advances have unveiled many environmental and genetic causes of fibrotic disorders, a better understanding of both ubiquitous and tissue-specific regulatory pathways and cellular dynamics could help to design new targeted therapies, and to identify the etiology of idiopathic diseases.
Within this Research Topic, we invite submission of articles (reviews, original research, or methodology articles) on the pathophysiological role of fibrosis and inflammation in different tissues. Areas to be covered include, but are not limited to:
- genetic and environmental causes of persistent low-level inflammation and fibrosis (e.g. autoimmunity, hypertension, obesity, diabetes, genetic diseases, latent infections);
- comorbidities including systemic sclerosis, neurological disorders, organ failure (heart, skeletal muscle, kidney, liver, lungs), cancer, and reduced resilience to infectious diseases;
- in vivo (animal models) and in vitro (organoids, tissue culture) modelling of fibrotic diseases for the discovery of novel therapeutic targets and potential tissue-specific treatments;
- vascular responses to inflammation and inflammation of vascular tissues;
- system biology approaches to identify molecular and cellular networks leading to chronic inflammation and fibrosis.
