About this Research Topic
Kidney disease is an emerging cause of morbidity and mortality. There are more than 6 million patients receiving renal replacement therapy worldwide. The global prevalence of chronic kidney disease (CKD) is between 11.7 and 15.1% of the adult population. Nevertheless, we still lack effective treatments to halt the progression of CKD making this an urgent area of unmet clinical need. CKD defined as abnormalities of kidney structure and/or function caused by primary and secondary glomerular diseases, including diabetes, hypertension, autoimmune disease, etc. Renal fibrosis is a common feature of CKD that is widely considered to be a major driving force in the progression to end-stage renal disease. However, the underlying mechanisms that induce the renal fibrotic response are complex and remain poorly understood. Emerging studies suggest that unresolved inflammation may be essential for driving the transition of acute kidney damage to chronic renal fibrosis.
Various leukocyte populations are recruited into the injured kidney and play important roles in pathogen clearance and tissue repair. However, if this inflammatory response does not resolve, it can paradoxically promote progressive fibrogenesis of the damaged kidney. Interestingly, numerous studies have revealed that kidney-infiltrating leukocytes, including macrophages, dendritic cells, natural killer cells and T and B cells; actively promote the transition of renal inflammation to fibrosis. In addition, alterations in the microenvironment in different kidney compartments also play a crucial role in the immune response and disease pathogenesis. Better understanding the immunologic processes in the development of CKD may uncover direct and indirect immunomodulatory approaches as novel therapeutic strategies for halting the progression of different forms of kidney disease.
This Research Topic focuses on the following areas:
1) Immunology in renal physiology and pathology
2) Pathogenic immunomodulators promoting the transition of renal inflammation into fibrosis
3) Novel immunotherapeutic targets for managing CKD
Reviews, Original Research Articles and Commentaries are welcome.
Topic Editor Dr. Patrick Tang holds patents related to anticancer therapy and diabetic prevention . All other Topic Editors declare no competing interests with regards to the Research Topic.
Various leukocyte populations are recruited into the injured kidney and play important roles in pathogen clearance and tissue repair. However, if this inflammatory response does not resolve, it can paradoxically promote progressive fibrogenesis of the damaged kidney. Interestingly, numerous studies have revealed that kidney-infiltrating leukocytes, including macrophages, dendritic cells, natural killer cells and T and B cells; actively promote the transition of renal inflammation to fibrosis. In addition, alterations in the microenvironment in different kidney compartments also play a crucial role in the immune response and disease pathogenesis. Better understanding the immunologic processes in the development of CKD may uncover direct and indirect immunomodulatory approaches as novel therapeutic strategies for halting the progression of different forms of kidney disease.
This Research Topic focuses on the following areas:
1) Immunology in renal physiology and pathology
2) Pathogenic immunomodulators promoting the transition of renal inflammation into fibrosis
3) Novel immunotherapeutic targets for managing CKD
Reviews, Original Research Articles and Commentaries are welcome.
Topic Editor Dr. Patrick Tang holds patents related to anticancer therapy and diabetic prevention . All other Topic Editors declare no competing interests with regards to the Research Topic.
Keywords: Inflammation, fibrosis, immunity, therapy, lncRNA
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