Diabetic nephropathy (DN) is an increasingly prevalent disease worldwide, and it's becoming the leading cause of end-stage renal disease, imposing a significant economic burden on society. The pathogenesis of DN is not yet entirely clear, but recent studies have shown that immunity and inflammation play a crucial role in its development. Even though DN isn't an immune complex-mediated renal disease, kidney intrinsic cells produce pro-inflammatory cytokines, promote immune response, and recruit macrophages and mast cells by releasing chemokines and cell adhesion molecules under diabetic stress. Through the activation of complement and recruitment of cytokines, the innate immune response is amplified, leading to the infiltration of inflammatory cells and mast cells in renal tissue and causing inflammatory injury and fibrosis of the kidney, resulting in a decline in the glomerular filtration rate. Animal and cell studies have confirmed that adaptive immune cells are also involved in the process of kidney injury induced by diabetes. Therefore, a better understanding of immune disorders and inflammatory responses in DN will help us develop new strategies for its diagnosis and treatment in humans.
Currently, there is no effective treatment for DN that can reduce albuminuria and glomerular filtration rate decline or prevent the development of end-stage renal disease. Clinical targeted immunity and inflammation therapy may provide new directions for future diagnosis and treatment. However, there are still many unanswered questions. The purpose of this topic is to focus on recent developments in inflammatory responses and immune disorders in DN, to determine the roles and mechanisms of inflammation and immunity in its development, and to provide new insights into its future diagnosis and treatment.
We welcome Original Research and Review manuscripts covering, but not limited to, the following subtopics:
1. The interaction between immune cells and inflammatory response in the occurrence and development of DN.
2. The involvement of innate and adaptive immunity in the process of kidney injury caused by diabetes.
3. Cellular signaling pathways causing inflammatory responses in DN.
4. Identifying inflammatory signaling pathways and mediators during the development, screening, and diagnosis of DN.
5. The role of inflammatory factors and immune biomarkers in the diagnosis and prognosis monitoring of DN.
6. The effects of current and new drugs for DN on inflammatory responses and immune disorders.
7. The application of existing and novel anti-inflammatory drugs and immunosuppressive drugs in the treatment of DN.
Diabetic nephropathy (DN) is an increasingly prevalent disease worldwide, and it's becoming the leading cause of end-stage renal disease, imposing a significant economic burden on society. The pathogenesis of DN is not yet entirely clear, but recent studies have shown that immunity and inflammation play a crucial role in its development. Even though DN isn't an immune complex-mediated renal disease, kidney intrinsic cells produce pro-inflammatory cytokines, promote immune response, and recruit macrophages and mast cells by releasing chemokines and cell adhesion molecules under diabetic stress. Through the activation of complement and recruitment of cytokines, the innate immune response is amplified, leading to the infiltration of inflammatory cells and mast cells in renal tissue and causing inflammatory injury and fibrosis of the kidney, resulting in a decline in the glomerular filtration rate. Animal and cell studies have confirmed that adaptive immune cells are also involved in the process of kidney injury induced by diabetes. Therefore, a better understanding of immune disorders and inflammatory responses in DN will help us develop new strategies for its diagnosis and treatment in humans.
Currently, there is no effective treatment for DN that can reduce albuminuria and glomerular filtration rate decline or prevent the development of end-stage renal disease. Clinical targeted immunity and inflammation therapy may provide new directions for future diagnosis and treatment. However, there are still many unanswered questions. The purpose of this topic is to focus on recent developments in inflammatory responses and immune disorders in DN, to determine the roles and mechanisms of inflammation and immunity in its development, and to provide new insights into its future diagnosis and treatment.
We welcome Original Research and Review manuscripts covering, but not limited to, the following subtopics:
1. The interaction between immune cells and inflammatory response in the occurrence and development of DN.
2. The involvement of innate and adaptive immunity in the process of kidney injury caused by diabetes.
3. Cellular signaling pathways causing inflammatory responses in DN.
4. Identifying inflammatory signaling pathways and mediators during the development, screening, and diagnosis of DN.
5. The role of inflammatory factors and immune biomarkers in the diagnosis and prognosis monitoring of DN.
6. The effects of current and new drugs for DN on inflammatory responses and immune disorders.
7. The application of existing and novel anti-inflammatory drugs and immunosuppressive drugs in the treatment of DN.
