Metabolic diseases, as a major public health burden, comprise obesity, atherosclerosis dyslipidemia, diabetes, hypertension, and hyperuricemia. Metabolic diseases are also accompanied with a bunch of cardiovascular risk factors that may foster the development and progression of kidney injuries. However, the mechanisms of metabolic disturbance-induced kidney diseases are not fully understood.
Chronic low-grade inflammation and activation of immune system are hallmarks of metabolic diseases. There is growing evidence that innate immune signaling modulates the development of metabolic diseases. Kidney as a target organ is often involved in the immune-mediated inflammation process. Meanwhile, molecules of the innate immune system regulate pathophysiological responses in multiple organs during metabolic disturbances, including disrupted metabolic homeostasis, tissue repair, and cell survival. The kidney harbors several classes of resident immune cells, whose activation and interaction with renal parenchymal cells upon kidney injury could also boost inflammatory response.
However, the assumption of immune-dependent signaling in metabolic disease-induced kidney diseases is mainly based on systemic inflammation. It remains unclear whether there is a kidney-specific immune response and how the systemic immune response interacts with the kidney. There are several renoprotective substances against the effects of metabolic diseases, but none of them directly targets the immune response.
The goal of this Research Topic is to provide a forum on advanced research focusing on metabolic disorder-induced immune inflammatory response in kidney diseases, as well as to explore the major regulators as intervention targets in the attempt to protect from metabolic kidney diseases. Manuscripts from the following subtopics are especially welcome:
1) Detection of immune-mediated inflammation and mechanisms on how immune system is activated by metabolic disorders in renal tissues
2) Elaboration on how activated immune response interacts with the kidney in the condition of metabolic disorders
3) Development and differentiation of immune cells mediated by non-epigenetic or epigenetic genes in metabolic kidney diseases
4) Judgement on whether the immunometabolism factors cause kidney disease development and progression, if so, how
5) Development of potential pharmacological intervention against immune inflammatory disorders in metabolic kidney diseases targeting non-epigenetic or epigenetic genes
Metabolic diseases, as a major public health burden, comprise obesity, atherosclerosis dyslipidemia, diabetes, hypertension, and hyperuricemia. Metabolic diseases are also accompanied with a bunch of cardiovascular risk factors that may foster the development and progression of kidney injuries. However, the mechanisms of metabolic disturbance-induced kidney diseases are not fully understood.
Chronic low-grade inflammation and activation of immune system are hallmarks of metabolic diseases. There is growing evidence that innate immune signaling modulates the development of metabolic diseases. Kidney as a target organ is often involved in the immune-mediated inflammation process. Meanwhile, molecules of the innate immune system regulate pathophysiological responses in multiple organs during metabolic disturbances, including disrupted metabolic homeostasis, tissue repair, and cell survival. The kidney harbors several classes of resident immune cells, whose activation and interaction with renal parenchymal cells upon kidney injury could also boost inflammatory response.
However, the assumption of immune-dependent signaling in metabolic disease-induced kidney diseases is mainly based on systemic inflammation. It remains unclear whether there is a kidney-specific immune response and how the systemic immune response interacts with the kidney. There are several renoprotective substances against the effects of metabolic diseases, but none of them directly targets the immune response.
The goal of this Research Topic is to provide a forum on advanced research focusing on metabolic disorder-induced immune inflammatory response in kidney diseases, as well as to explore the major regulators as intervention targets in the attempt to protect from metabolic kidney diseases. Manuscripts from the following subtopics are especially welcome:
1) Detection of immune-mediated inflammation and mechanisms on how immune system is activated by metabolic disorders in renal tissues
2) Elaboration on how activated immune response interacts with the kidney in the condition of metabolic disorders
3) Development and differentiation of immune cells mediated by non-epigenetic or epigenetic genes in metabolic kidney diseases
4) Judgement on whether the immunometabolism factors cause kidney disease development and progression, if so, how
5) Development of potential pharmacological intervention against immune inflammatory disorders in metabolic kidney diseases targeting non-epigenetic or epigenetic genes
