Many signalling pathways have been shown to be involved in the progression of kidney disease in humans and in animal models, usually due to persistent activation of these pathways. Perhaps the best well known of such pathways include certain inflammatory cytokines and protein kinase pathways, such as protein kinase C and mitogen-activated kinase pathways, which lead to cellular growth and fibrosis. Additionally, pathways such as angiotensin II and transforming growth factor-ß signaling pathways, which enhance fibrosis leads to kidney scarring. Therefore, challenges in kidney disease include continuing to improve the advances in pathogenesis and molecular biology, and novel therapeutic options.
This Research Topic aims to update important aspects regarding kidney disease such as diabetic nephropathy, lupus nephritis, and vasculitis nephritis (i.e. anti-neutrophilic cytoplasmic antibodies associated vasculitis). We also aim to discuss new disease targets, description of potential pathologic pathways, and promising therapeutic approaches from basic science to clinical work.
Details for authors: Investigators working on animal models of renal injury such as autoimmune nephritis and clinical studies in these areas are encouraged to submit their work. For these purposes, we intend to include original, review and perspective articles, and commentaries. We hope this Research Topic will provide a broad update in several kidney diseases and will determine relevant advances in different aspects in the field. We do not encourage the submission of case reports unless they are in the context of a comprehensive review of relevant literature that may lead to changes in practice and treatment approaches.
Many signalling pathways have been shown to be involved in the progression of kidney disease in humans and in animal models, usually due to persistent activation of these pathways. Perhaps the best well known of such pathways include certain inflammatory cytokines and protein kinase pathways, such as protein kinase C and mitogen-activated kinase pathways, which lead to cellular growth and fibrosis. Additionally, pathways such as angiotensin II and transforming growth factor-ß signaling pathways, which enhance fibrosis leads to kidney scarring. Therefore, challenges in kidney disease include continuing to improve the advances in pathogenesis and molecular biology, and novel therapeutic options.
This Research Topic aims to update important aspects regarding kidney disease such as diabetic nephropathy, lupus nephritis, and vasculitis nephritis (i.e. anti-neutrophilic cytoplasmic antibodies associated vasculitis). We also aim to discuss new disease targets, description of potential pathologic pathways, and promising therapeutic approaches from basic science to clinical work.
Details for authors: Investigators working on animal models of renal injury such as autoimmune nephritis and clinical studies in these areas are encouraged to submit their work. For these purposes, we intend to include original, review and perspective articles, and commentaries. We hope this Research Topic will provide a broad update in several kidney diseases and will determine relevant advances in different aspects in the field. We do not encourage the submission of case reports unless they are in the context of a comprehensive review of relevant literature that may lead to changes in practice and treatment approaches.
