Inflammation represents a multi-faced condition in between the health and disease. It is well accepted, and verified, that while a correct control of the inflammatory phase is crucial for a correct healing process, a sustained long-lasting phase may trigger pathogenic changes including cell trans-differentiation and fibrosis. The control of inflammation is complex, being constituted by reciprocally regulated mechanisms finely tuned by humoral and tissue factors working with paracrine and endocrine mechanisms. The overall result is an inflammatory condition that may be clinically detectable or restrained at sub-clinical levels. The latter condition is recognized as the common ground of several cardiac and metabolic chronic diseases. Because of this, the early detection of some inflammatory markers and the identification of novel inflammatory mechanisms still represents a challenge for basic and clinical research aiming at the prevention and the care of chronic heart and metabolic diseases.
Inflammation is usually induced by tissue invasion from inflammatory cells including leukocytes, mast cells and macrophages. Once in the tissues, these cells become activated releasing pro-inflammatory factors of different nature, which, by activating their respective targets, may produce modification in tissue/cell secretome, metabolism and/or induce phenotypic modifications.
The adipose tissue and the heart have different function and anatomical localization but they are both reciprocally and homeostatically regulated. In fact, several lines of evidence indicate that an healthy adipose tissue is essential for an healthy heart and when the adipose tissue gets sick, secondary to a massive inflammatory cell infiltration, its incorrected endocrine/paracrine activity represents a risk factor for cardiovascular diseases, including obesity, diabetes and atrial fibrillation. However, evidence also indicate that in some conditions, the heart and the adipose tissue may became anatomically close. In particular, the adipose tissue may infiltrate the epicardial layer or the intima of cardiac vessels. The infiltrating adipose tissue is a sick tissue and its sickness is transmitted to the heart which is now a new organ, the fat-heart.
Based on the above, this Research Topic aims to collect and discuss the actual knowledge on the mechanisms producing inflammatory cell infiltration of the fat, of the heart and of the fat-heart, the consequence of such infiltration on tissue function and to focus on the role of pharmacological control of inflammatory mediators levels and of their targets with particular emphasis to receptors activated by serine proteases.
This Research Topic is specifically interested in original research, commentary and review and articles.
Inflammation represents a multi-faced condition in between the health and disease. It is well accepted, and verified, that while a correct control of the inflammatory phase is crucial for a correct healing process, a sustained long-lasting phase may trigger pathogenic changes including cell trans-differentiation and fibrosis. The control of inflammation is complex, being constituted by reciprocally regulated mechanisms finely tuned by humoral and tissue factors working with paracrine and endocrine mechanisms. The overall result is an inflammatory condition that may be clinically detectable or restrained at sub-clinical levels. The latter condition is recognized as the common ground of several cardiac and metabolic chronic diseases. Because of this, the early detection of some inflammatory markers and the identification of novel inflammatory mechanisms still represents a challenge for basic and clinical research aiming at the prevention and the care of chronic heart and metabolic diseases.
Inflammation is usually induced by tissue invasion from inflammatory cells including leukocytes, mast cells and macrophages. Once in the tissues, these cells become activated releasing pro-inflammatory factors of different nature, which, by activating their respective targets, may produce modification in tissue/cell secretome, metabolism and/or induce phenotypic modifications.
The adipose tissue and the heart have different function and anatomical localization but they are both reciprocally and homeostatically regulated. In fact, several lines of evidence indicate that an healthy adipose tissue is essential for an healthy heart and when the adipose tissue gets sick, secondary to a massive inflammatory cell infiltration, its incorrected endocrine/paracrine activity represents a risk factor for cardiovascular diseases, including obesity, diabetes and atrial fibrillation. However, evidence also indicate that in some conditions, the heart and the adipose tissue may became anatomically close. In particular, the adipose tissue may infiltrate the epicardial layer or the intima of cardiac vessels. The infiltrating adipose tissue is a sick tissue and its sickness is transmitted to the heart which is now a new organ, the fat-heart.
Based on the above, this Research Topic aims to collect and discuss the actual knowledge on the mechanisms producing inflammatory cell infiltration of the fat, of the heart and of the fat-heart, the consequence of such infiltration on tissue function and to focus on the role of pharmacological control of inflammatory mediators levels and of their targets with particular emphasis to receptors activated by serine proteases.
This Research Topic is specifically interested in original research, commentary and review and articles.
