Caveolins belong to a family of proteins enriched in caveolae, which are invaginations of the cell that constitute a specific type of lipid rafts. Caveolin-1 and -2 are ubiquitously expressed. Cells like adipocytes, endothelial cells, fibroblasts and type I pneumocytes exhibit a high expression of caveolin-1, whereas cells like macrophages show a low level of caveolin-1 that is highly increased upon inflammatory stimuli. Caveolin-3 is found in striated muscle mainly. Caveolin-1 and -3 are essential for caveolae formation, while caveolin-2 is not and depends on caveolin-1 for oligomerization and caveolae formation. Caveolin-1 is by far the most studied member of this family. Beyond caveolae, it is found in various organelles, such as endosomes, lysosomes, Golgi, nucleus, mitochondria, and lipid droplets. Caveolin-1 is a fascinating molecule able to interact with lipids and a myriad of proteins. It is considered a scaffold protein that organizes signal transduction in the cell. Interaction with caveolin-1 can sequester proteins to caveolae, regulate their activities or address them to degradation. As a high-affinity cholesterol-binding protein, caveolin-1 affects the cell lipid metabolism and vesicular traffic. Caveolin-3 is specific to skeletal muscle and shares many properties with caveolin-1. Caveolin-2 is the most divergent member of the family. It is the less studied member of the family and the amount of information about its activities is small compared to the large knowledge gathered about caveolin-1 so far.
There are knockout mice for all caveolins, meaning they are not essential for life. However, the absence of these proteins is associated with a broad panel of disturbances that predispose mice to the development of several diseases, depending on the triggering stimulus. Caveolin knockout mice helped elucidate many mechanisms of disease development that may translate to human conditions. Mutations in caveolin genes and altered levels of wild-type caveolin proteins are associated with several human diseases, such as cancer, muscular dystrophy, and diabetes type II. An important aspect of caveolin activity in diseases is its ability to control the inflammatory response because inflammation underlies a vast array of human disorders. In infectious diseases, caveolins act as a double-edged sword, favoring either the infectious agent or the host. Therefore, caveolins can be a therapeutic target for treating some types of disorders.
The aim of this Research Topic is to provide a spectrum of scenarios on how caveolins act in the regulation of inflammatory responses that underlie homeostasis control and disease development. In particular, we want to shed light on the roles of this multifaceted molecule, which may help elucidate the intricate regulatory process of inflammation. Our call for papers includes studies using distinct approaches such as in vitro models, animal models, and clinical data. We welcome submissions of Original Research, Reviews, Mini-Reviews, and Perspectives articles discussing caveolin-mediated mechanisms in the context of:
- Extracellular vesicles regulation
- Fibrosis
- Infection
- Inflammation
- Metabolism
- Sepsis
Only manuscripts that focus on the protein caveolin-1 will be accepted for submission to this special Research Topic collection.
Topic Editor Prof. Stanley Hoffman is the founder and CEO of FibroTherapeutics Inc. and holds a patent on CSD in fibrotic disease licensed to the company Lung Therapeutics. The other Topic Editors declare no competing interests with regard to the Research Topic subject.
Caveolins belong to a family of proteins enriched in caveolae, which are invaginations of the cell that constitute a specific type of lipid rafts. Caveolin-1 and -2 are ubiquitously expressed. Cells like adipocytes, endothelial cells, fibroblasts and type I pneumocytes exhibit a high expression of caveolin-1, whereas cells like macrophages show a low level of caveolin-1 that is highly increased upon inflammatory stimuli. Caveolin-3 is found in striated muscle mainly. Caveolin-1 and -3 are essential for caveolae formation, while caveolin-2 is not and depends on caveolin-1 for oligomerization and caveolae formation. Caveolin-1 is by far the most studied member of this family. Beyond caveolae, it is found in various organelles, such as endosomes, lysosomes, Golgi, nucleus, mitochondria, and lipid droplets. Caveolin-1 is a fascinating molecule able to interact with lipids and a myriad of proteins. It is considered a scaffold protein that organizes signal transduction in the cell. Interaction with caveolin-1 can sequester proteins to caveolae, regulate their activities or address them to degradation. As a high-affinity cholesterol-binding protein, caveolin-1 affects the cell lipid metabolism and vesicular traffic. Caveolin-3 is specific to skeletal muscle and shares many properties with caveolin-1. Caveolin-2 is the most divergent member of the family. It is the less studied member of the family and the amount of information about its activities is small compared to the large knowledge gathered about caveolin-1 so far.
There are knockout mice for all caveolins, meaning they are not essential for life. However, the absence of these proteins is associated with a broad panel of disturbances that predispose mice to the development of several diseases, depending on the triggering stimulus. Caveolin knockout mice helped elucidate many mechanisms of disease development that may translate to human conditions. Mutations in caveolin genes and altered levels of wild-type caveolin proteins are associated with several human diseases, such as cancer, muscular dystrophy, and diabetes type II. An important aspect of caveolin activity in diseases is its ability to control the inflammatory response because inflammation underlies a vast array of human disorders. In infectious diseases, caveolins act as a double-edged sword, favoring either the infectious agent or the host. Therefore, caveolins can be a therapeutic target for treating some types of disorders.
The aim of this Research Topic is to provide a spectrum of scenarios on how caveolins act in the regulation of inflammatory responses that underlie homeostasis control and disease development. In particular, we want to shed light on the roles of this multifaceted molecule, which may help elucidate the intricate regulatory process of inflammation. Our call for papers includes studies using distinct approaches such as in vitro models, animal models, and clinical data. We welcome submissions of Original Research, Reviews, Mini-Reviews, and Perspectives articles discussing caveolin-mediated mechanisms in the context of:
- Extracellular vesicles regulation
- Fibrosis
- Infection
- Inflammation
- Metabolism
- Sepsis
Only manuscripts that focus on the protein caveolin-1 will be accepted for submission to this special Research Topic collection.
Topic Editor Prof. Stanley Hoffman is the founder and CEO of FibroTherapeutics Inc. and holds a patent on CSD in fibrotic disease licensed to the company Lung Therapeutics. The other Topic Editors declare no competing interests with regard to the Research Topic subject.
