Obesity and the associated risks of metabolic diseases including Type 2 Diabetes mellitus (T2DM), nonalcoholic fatty liver disease (NAFLD), steatohepatitis, asthma, cancer, and cardiovascular diseases (CVD) have become a global epidemic, which poses formidable challenges to human health. Adipose tissue (AT) is particularly important for energy storage and could greatly expand in response to overnutrition and store those excess nutrients as triglycerides. However, in most cases, AT ultimately reach a threshold that the anabolic pressure cannot be further accommodated, which creates stress on adipocytes and triggers an inflammatory program through multiple initiators. Evidence has shown that obesity is closely associated with AT inflammation while the degree of inflammation correlates well with the severity of insulin resistance and T2DM. Thus, understanding the inflammatory response of AT might lead to the development of new approaches to treating these devastating diseases.
While the recent advance in gene-editing-based studies has greatly extended our understanding of AT inflammation in the past decades, the complex and exquisite regulation of AT inflammation decision in various physiological and pathological conditions of metabolic diseases continues to fascinate researchers of the field. The development of new technologies, especially high-throughput single-cell omics analysis and high-resolution metabolomics, has provided new insights into the cellular and molecular mechanisms that govern AT inflammation, and how these inflammatory responses are correlated with energy homeostasis. Thus, this Research Topic aims to further highlight new discoveries on the molecular and cellular basis of AT inflammation, especially those during the pathology of metabolic diseases. We prospect new progress to be made in the complex interplay between AT inflammation and metabolic diseases, to illustrate how extrinsic factors such as nutritional status alters the intrinsic signaling pathways and genetic regulatory network of AT inflammation to control energy homeostasis.
This Research Topic is intended to provide readers the basic research on the important role of AT in energy homeostasis, detailing the changes in AT inflammation that lead to some of the deleterious effects of obesity-associated metabolic diseases, discovering the cellular and molecular triggers for obesity-induced inflammation and discuss potential therapeutic approaches for addressing this problem. We welcome Original research, Review, Mini-Review, Short communications, and Perspectives articles that are related, but not limited to the following subtopics:
· Characterization of AT inflammation in diseases.
· Function of immune cells and their derived cytokines in AT.
· Adipocyte-derived cytokines in energy metabolism.
· Microenvironmental control of adipocyte fate and function.
· Metabolite associated with AT inflammation.
· Immune cell and adipocyte crosstalk.
· Potential therapeutic strategies to target inflammation in AT.
Obesity and the associated risks of metabolic diseases including Type 2 Diabetes mellitus (T2DM), nonalcoholic fatty liver disease (NAFLD), steatohepatitis, asthma, cancer, and cardiovascular diseases (CVD) have become a global epidemic, which poses formidable challenges to human health. Adipose tissue (AT) is particularly important for energy storage and could greatly expand in response to overnutrition and store those excess nutrients as triglycerides. However, in most cases, AT ultimately reach a threshold that the anabolic pressure cannot be further accommodated, which creates stress on adipocytes and triggers an inflammatory program through multiple initiators. Evidence has shown that obesity is closely associated with AT inflammation while the degree of inflammation correlates well with the severity of insulin resistance and T2DM. Thus, understanding the inflammatory response of AT might lead to the development of new approaches to treating these devastating diseases.
While the recent advance in gene-editing-based studies has greatly extended our understanding of AT inflammation in the past decades, the complex and exquisite regulation of AT inflammation decision in various physiological and pathological conditions of metabolic diseases continues to fascinate researchers of the field. The development of new technologies, especially high-throughput single-cell omics analysis and high-resolution metabolomics, has provided new insights into the cellular and molecular mechanisms that govern AT inflammation, and how these inflammatory responses are correlated with energy homeostasis. Thus, this Research Topic aims to further highlight new discoveries on the molecular and cellular basis of AT inflammation, especially those during the pathology of metabolic diseases. We prospect new progress to be made in the complex interplay between AT inflammation and metabolic diseases, to illustrate how extrinsic factors such as nutritional status alters the intrinsic signaling pathways and genetic regulatory network of AT inflammation to control energy homeostasis.
This Research Topic is intended to provide readers the basic research on the important role of AT in energy homeostasis, detailing the changes in AT inflammation that lead to some of the deleterious effects of obesity-associated metabolic diseases, discovering the cellular and molecular triggers for obesity-induced inflammation and discuss potential therapeutic approaches for addressing this problem. We welcome Original research, Review, Mini-Review, Short communications, and Perspectives articles that are related, but not limited to the following subtopics:
· Characterization of AT inflammation in diseases.
· Function of immune cells and their derived cytokines in AT.
· Adipocyte-derived cytokines in energy metabolism.
· Microenvironmental control of adipocyte fate and function.
· Metabolite associated with AT inflammation.
· Immune cell and adipocyte crosstalk.
· Potential therapeutic strategies to target inflammation in AT.
