Diabetes mellitus causes stimulation of receptor mediated signalling pathways, that lead to outcomes resulting in organ fibrosis such as the kidneys, heart and vessels. Nearly 25% of diabetic people eventually develop kidney disease. The molecular and cellular mechanisms of this renal disease are poorly understood. Destruction of cellular structures, deposition of extracellular matrix, release of inflammatory cytokines and inductions of trans-differentiation processes in diabetes are the key phenomenon that influences fibrogenic pathways.
This series studies mechanisms that demonstrate the protective role of glucocorticoid receptors and fibroblast-growth factor receptor 1 signaling in the diabetic vascular endothelial cells which are known to inhibit the defective central metabolism-linked endothelial-to-mesenchymal transitions in diabetic kidneys and the heart whereas, dipeptidyl transpeptidase-4 and low-density lipoprotein receptor-related protein 5 and 6 are key mesenchymal inducers in diabetic epithelial and vascular endothelial cells.
Improved understanding of the pathogenesis of diabetes and associated complication is urgently needed to catalyze the development of new therapeutics. In this advancement, we can identify new chemical entities, pharmacological agents and pharmacophores which influences the receptors mediated cell signaling in diverse cell types. In addition, new mechanisms or pathways will be evaluated for their organ-protective abilities in diabetes.
This is the second volume to the successful Research Topic in Renal Pharmacology, we are inviting original as well as review articles from both previous authors and new contributors to provide deeper insight into topics relating to but not limited to the following areas:
• New pathophysiologic pathways
• Cell surface receptors, nuclear receptors, cell junction proteins and development of their agonist and antagonists in the management of diabetic associated complications.
Diabetes mellitus causes stimulation of receptor mediated signalling pathways, that lead to outcomes resulting in organ fibrosis such as the kidneys, heart and vessels. Nearly 25% of diabetic people eventually develop kidney disease. The molecular and cellular mechanisms of this renal disease are poorly understood. Destruction of cellular structures, deposition of extracellular matrix, release of inflammatory cytokines and inductions of trans-differentiation processes in diabetes are the key phenomenon that influences fibrogenic pathways.
This series studies mechanisms that demonstrate the protective role of glucocorticoid receptors and fibroblast-growth factor receptor 1 signaling in the diabetic vascular endothelial cells which are known to inhibit the defective central metabolism-linked endothelial-to-mesenchymal transitions in diabetic kidneys and the heart whereas, dipeptidyl transpeptidase-4 and low-density lipoprotein receptor-related protein 5 and 6 are key mesenchymal inducers in diabetic epithelial and vascular endothelial cells.
Improved understanding of the pathogenesis of diabetes and associated complication is urgently needed to catalyze the development of new therapeutics. In this advancement, we can identify new chemical entities, pharmacological agents and pharmacophores which influences the receptors mediated cell signaling in diverse cell types. In addition, new mechanisms or pathways will be evaluated for their organ-protective abilities in diabetes.
This is the second volume to the successful Research Topic in Renal Pharmacology, we are inviting original as well as review articles from both previous authors and new contributors to provide deeper insight into topics relating to but not limited to the following areas:
• New pathophysiologic pathways
• Cell surface receptors, nuclear receptors, cell junction proteins and development of their agonist and antagonists in the management of diabetic associated complications.
